PMID- 20977075 OWN - NLM STAT- MEDLINE DA - 20101027 DCOM- 20101109 IS - 0350-6134 (Print) IS - 0350-6134 (Linking) VI - 34 IP - 3 DP - 2010 Sep TI - Screening with mammography organized by family physicians teams: what have we learnt? PG - 871-6 AB - The mammography, recommended as standard method for screening on breast cancer, can reveal suspicious lesions early enough to anable cancer elimination in entirely. Experience with women of the target population, 50-69 years old, included in the mass screening programs, show the reduction in the specific mortality by 30%. One of the main problem in organizing the preventive programs is how to increase responsiveness of subjects to screening. In the study, based on the large sample of over 1000 of subjects and 20 family medicine practices, included in the investigation, we showed that it is possible, by a pro-active involvement of family physicians teams and intensive educational and motivational activities, to achieve high level of over 80% of responsiveness to mammography screening. Analysis of the reasons of nonresponsiveness can contribute to better understanding of the mental processes included in a self-decision making. This, as the final aim, can help family physicians in their efforts to overcome many hidden barriers which obstruct their patients to accept the mammography screening. AD - School of Medicine, Josip Juraj Strossmayer University, Osijek, Croatia. sanda.pribic@os.t-com.hr FAU - Pribic, Sanda AU - Pribic S FAU - Gmajnic, Rudika AU - Gmajnic R FAU - Majnaric-Trtica, Ljiljana AU - Majnaric-Trtica L FAU - Ebling, Barbara AU - Ebling B FAU - Vranjei, Zeljko AU - Vranjei Z LA - eng PT - Journal Article PL - Croatia TA - Coll Antropol JT - Collegium antropologicum JID - 8003354 SB - IM MH - Aged MH - Breast Neoplasms/*prevention & control/radiography MH - Croatia/epidemiology MH - Family Practice MH - Female MH - Humans MH - *Mammography MH - *Mass Screening MH - Middle Aged EDAT- 2010/10/28 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/10/28 06:00 PST - ppublish SO - Coll Antropol. 2010 Sep;34(3):871-6. PMID- 20975037 OWN - NLM STAT- MEDLINE DA - 20101103 DCOM- 20101116 IS - 1460-2105 (Electronic) IS - 0027-8874 (Linking) VI - 102 IP - 21 DP - 2010 Nov 3 TI - Cancer risks after radiation exposure in middle age. PG - 1628-36 AB - BACKGROUND: Epidemiological data show that radiation exposure during childhood is associated with larger cancer risks compared with exposure at older ages. For exposures in adulthood, however, the relative risks of radiation-induced cancer in Japanese atomic bomb survivors generally do not decrease monotonically with increasing age of adult exposure. These observations are inconsistent with most standard models of radiation-induced cancer, which predict that relative risks decrease monotonically with increasing age at exposure, at all ages. METHODS: We analyzed observed cancer risk patterns as a function of age at exposure in Japanese atomic bomb survivors by using a biologically based quantitative model of radiation carcinogenesis that incorporates both radiation induction of premalignant cells (initiation) and radiation-induced promotion of premalignant damage. This approach emphasizes the kinetics of radiation-induced initiation and promotion, and tracks the yields of premalignant cells before, during, shortly after, and long after radiation exposure. RESULTS: Radiation risks after exposure in younger individuals are dominated by initiation processes, whereas radiation risks after exposure at later ages are more influenced by promotion of preexisting premalignant cells. Thus, the cancer site-dependent balance between initiation and promotion determines the dependence of cancer risk on age at radiation exposure. For example, in terms of radiation induction of premalignant cells, a quantitative measure of the relative contribution of initiation vs promotion is 10-fold larger for breast cancer than for lung cancer. Reflecting this difference, radiation-induced breast cancer risks decrease with age at exposure at all ages, whereas radiation-induced lung cancer risks do not. CONCLUSION: For radiation exposure in middle age, most radiation-induced cancer risks do not, as often assumed, decrease with increasing age at exposure. This observation suggests that promotional processes in radiation carcinogenesis become increasingly important as the age at exposure increases. Radiation-induced cancer risks after exposure in middle age may be up to twice as high as previously estimated, which could have implications for occupational exposure and radiological imaging. AD - Center for Radiological Research, Department of Radiation Oncology, Columbia University Medical Center, New York, NY, USA. FAU - Shuryak, Igor AU - Shuryak I FAU - Sachs, Rainer K AU - Sachs RK FAU - Brenner, David J AU - Brenner DJ LA - eng GR - U19-AI67773/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, U.S. Gov't, Non-P.H.S. DEP - 20101025 PL - United States TA - J Natl Cancer Inst JT - Journal of the National Cancer Institute JID - 7503089 SB - IM CIN - J Natl Cancer Inst. 2010 Nov 3;102(21):1606-9. PMID: 20975038 MH - Adult MH - Advisory Committees MH - Age Factors MH - Aged MH - Asian Continental Ancestry Group/*statistics & numerical data MH - Breast Neoplasms/epidemiology/etiology MH - Cell Transformation, Neoplastic/*radiation effects MH - Confounding Factors (Epidemiology) MH - Dose-Response Relationship, Radiation MH - Female MH - Humans MH - Incidence MH - Japan/epidemiology MH - Lung Neoplasms/epidemiology/etiology MH - Male MH - Middle Aged MH - Neoplasms, Radiation-Induced/*epidemiology/*etiology/mortality MH - *Nuclear Warfare MH - Precancerous Conditions/pathology MH - Risk Assessment MH - Risk Factors MH - Survivors/*statistics & numerical data MH - World War II PMC - PMC2970575 OID - NLM: PMC2970575 [Available on 11/03/11] EDAT- 2010/10/27 06:00 MHDA- 2010/11/17 06:00 CRDT- 2010/10/27 06:00 PMCR- 2011/11/03 PHST- 2010/10/25 [aheadofprint] AID - djq346 [pii] AID - 10.1093/jnci/djq346 [doi] PST - ppublish SO - J Natl Cancer Inst. 2010 Nov 3;102(21):1628-36. Epub 2010 Oct 25. PMID- 20975025 OWN - NLM STAT- MEDLINE DA - 20101026 DCOM- 20101109 IS - 1538-3679 (Electronic) IS - 0003-9926 (Linking) VI - 170 IP - 19 DP - 2010 Oct 25 TI - Physical activity and risk of breast cancer among postmenopausal women. PG - 1758-64 AB - BACKGROUND: Physical activity has many health benefits. Although greater activity has been related to lower postmenopausal breast cancer risk, important details remain unclear, including type, intensity, and timing of activity and whether the association varies by subgroups. METHODS: Within the prospective Nurses' Health Study, we assessed the associations of specific and total activity, queried every 2 to 4 years since 1986, with breast cancer risk. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Activity was measured as hours of metabolic equivalent task values (MET-h). RESULTS: During 20 years of follow-up (1986-2006), 4782 invasive breast cancer cases were documented among 95 396 postmenopausal women. Compared with less than 3 MET-h/wk (<1 h/wk walking), women engaged in higher amounts of recent total physical activity were at lower breast cancer risk (>/=27 MET-h/wk [approximately 1 h/d of brisk walking]: HR, 0.85; 95% CI, 0.78-0.93; P < .001 for trend). Compared with women who were least active at menopause and through follow-up (<9 MET-h/wk [approximately 30 minutes of walking at an average pace on most days of the week]), women who increased activity were at lower risk (<9 MET-h/wk at menopause and >/=9 MET-h/wk during follow-up: HR, 0.90; 95% CI, 0.82-0.98). Among specific activities modeled simultaneously, brisk walking was associated with lower risk (per 20 MET-h/wk [5 h/wk]: HR, 0.91; 95% CI, 0.84-0.98). The association with total activity did not differ significantly between estrogen and progesterone receptor-positive and -negative tumors (P = .65 for heterogeneity). CONCLUSION: Our findings suggest that moderate physical activity, including brisk walking, may reduce postmenopausal breast cancer risk and that increases in activity after menopause may be beneficial. AD - Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. heather.eliassen@channing.harvard.edu FAU - Eliassen, A Heather AU - Eliassen AH FAU - Hankinson, Susan E AU - Hankinson SE FAU - Rosner, Bernard AU - Rosner B FAU - Holmes, Michelle D AU - Holmes MD FAU - Willett, Walter C AU - Willett WC LA - eng GR - CA87969/CA/NCI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, N.I.H., Extramural PL - United States TA - Arch Intern Med JT - Archives of internal medicine JID - 0372440 SB - AIM SB - IM MH - Adult MH - Breast Neoplasms/*epidemiology/prevention & control MH - Confidence Intervals MH - Exercise/*physiology MH - Female MH - Follow-Up Studies MH - Humans MH - Incidence MH - Middle Aged MH - Postmenopause/*physiology MH - Proportional Hazards Models MH - Prospective Studies MH - Questionnaires MH - Risk Factors MH - United States/epidemiology EDAT- 2010/10/27 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/10/27 06:00 AID - 170/19/1758 [pii] AID - 10.1001/archinternmed.2010.363 [doi] PST - ppublish SO - Arch Intern Med. 2010 Oct 25;170(19):1758-64. PMID- 20944177 OWN - NLM STAT- MEDLINE DA - 20101014 DCOM- 20101110 IS - 1791-7530 (Electronic) IS - 0250-7005 (Linking) VI - 30 IP - 9 DP - 2010 Sep TI - Psychological response to cancer: role of 5-HTTLPR genetic polymorphism of serotonin transporter. PG - 3823-6 AB - BACKGROUND: 5-HTTLPR genetic polymorphism of serotonin transporter (SERT) and stressful life events facilitate depression. The aim of this investigation was therefore to determine the correlations between SERT polymorphism and mental adjustment to cancer. PATIENTS AND METHODS: Breast cancer patients early after surgery, and subjects with various advanced tumours were recruited, evaluated using the Mini Mental Adjustment to Cancer Scale and Hospital Anxiety and Depression Scale (HADS), and genotyped. RESULTS: In early breast cancer patients (n=53), hopelessness-helplessness (HH) and anxious preoccupation (AP) significantly correlated with depression and anxiety; avoidance (AV) correlated with anxiety. Advanced cancer patients (n=73) displayed similar correlations, and a negative correlation of HADS depression with fighting spirit (FS) and AV. The stratification for 5-HTTLPR showed that early breast cancer carriers of the L/L variant displayed a significant correlation between HH and depression. CONCLUSION: Among early breast cancer patients, a specific set, characterized by their 5-HTTLPR variant, display differential correlations between HH and depression, with possible implications for treatment options. AD - Department of Life Sciences, University of Trieste, 34127 Trieste, Italy. FAU - Schillani, Giulia AU - Schillani G FAU - Martinis, Elisabetta AU - Martinis E FAU - Capozzo, Maria Anna AU - Capozzo MA FAU - Era, Daniel AU - Era D FAU - Cristante, Tania AU - Cristante T FAU - Mustacchi, Giorgio AU - Mustacchi G FAU - Conte, Maria Anna AU - Conte MA FAU - DE Vanna, Maurizio AU - DE Vanna M FAU - Grassi, Luigi AU - Grassi L FAU - Giraldi, Tullio AU - Giraldi T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Greece TA - Anticancer Res JT - Anticancer research JID - 8102988 RN - 0 (SLC6A4 protein, human) RN - 0 (Serotonin Plasma Membrane Transport Proteins) SB - IM MH - Adaptation, Psychological/physiology MH - Anxiety/genetics MH - Breast Neoplasms/*genetics/*psychology MH - Depression/genetics MH - Female MH - *Genetic Predisposition to Disease MH - Humans MH - *Polymorphism, Single Nucleotide MH - Serotonin Plasma Membrane Transport Proteins/*genetics EDAT- 2010/10/15 06:00 MHDA- 2010/11/11 06:00 CRDT- 2010/10/15 06:00 AID - 30/9/3823 [pii] PST - ppublish SO - Anticancer Res. 2010 Sep;30(9):3823-6. PMID- 20944124 OWN - NLM STAT- MEDLINE DA - 20101014 DCOM- 20101110 IS - 1791-7530 (Electronic) IS - 0250-7005 (Linking) VI - 30 IP - 9 DP - 2010 Sep TI - Down-regulation of heat-shock protein 70 (HSP-70) correlated with responsiveness to neoadjuvant aromatase inhibitor therapy in breast cancer patients. PG - 3465-72 AB - BACKGROUND: Aromatase inhibitor (AI) has been established as an effective endocrine therapy in estrogen receptor (ER)-positive postmenopausal breast cancer patients. Our recent proteomic analysis demonstrated that ten proteins were significantly altered in their expression levels before and after the therapy in the patients receiving neoadjuvant AI. Among these newly identified proteins, heat-shock protein 70 (HSP-70) was the most significantly correlated with both clinical and pathological responses. Therefore, in this study, we further evaluated the significance of this HSP-70 alteration using immunohistochemistry. MATERIALS AND METHODS: A total of 32 patients treated with neoadjuvant exemestane or letrozole in whom pre- and post-treatment tumor tissues were available were included. Immunohistochemical evaluation of ER, progesterone receptor (PgR), Her-2, Ki-67 and HSP-70 was performed. Results obtained were compared to both clinical and biological responses of the patients. RESULTS: The majority of the patients responded to treatment (16 patients with partial response, 14 with stable disease and 2 with progressive disease). The means of ER, Ki-67 and HSP-70 were significantly different between treatment responders and non-responders. Decrement of HSP-70 and Ki-67 after AI treatment and pretreatment Ki-67 labeling index of >10% tumor cells were significantly associated with clinical responsiveness to AI treatment (p<0.0001). There was a significant positive correlation between changes of HSP-70 and Ki-67 before and after the therapy. CONCLUSION: Decrement of HSP-70 in breast carcinoma cells plays important roles in therapeutic mechanisms of AIs through suppressing tumor cell proliferation in breast cancer patients. AD - Department of Pathology, Tohoku University School of Medicine, Sendai, Japan. FAU - Yiu, Christopher C P AU - Yiu CC FAU - Chanplakorn, Niramol AU - Chanplakorn N FAU - Chan, Monica S M AU - Chan MS FAU - Loo, Wings T Y AU - Loo WT FAU - Chow, Louis W C AU - Chow LW FAU - Toi, Masakazu AU - Toi M FAU - Sasano, Hironobu AU - Sasano H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Greece TA - Anticancer Res JT - Anticancer research JID - 8102988 RN - 0 (Androstadienes) RN - 0 (Antineoplastic Agents) RN - 0 (Aromatase Inhibitors) RN - 0 (HSP70 Heat-Shock Proteins) RN - 0 (Ki-67 Antigen) RN - 0 (Nitriles) RN - 0 (Triazoles) RN - 107868-30-4 (exemestane) RN - 112809-51-5 (letrozole) SB - IM MH - Aged MH - Androstadienes/therapeutic use MH - Antineoplastic Agents/therapeutic use MH - Aromatase Inhibitors/*therapeutic use MH - Breast Neoplasms/*drug therapy/metabolism MH - Down-Regulation MH - Drug Resistance, Neoplasm/*physiology MH - Female MH - HSP70 Heat-Shock Proteins/*biosynthesis MH - Humans MH - Immunohistochemistry MH - Ki-67 Antigen/biosynthesis MH - *Neoadjuvant Therapy MH - Nitriles/therapeutic use MH - Randomized Controlled Trials as Topic MH - Triazoles/therapeutic use EDAT- 2010/10/15 06:00 MHDA- 2010/11/11 06:00 CRDT- 2010/10/15 06:00 AID - 30/9/3465 [pii] PST - ppublish SO - Anticancer Res. 2010 Sep;30(9):3465-72. PMID- 20944121 OWN - NLM STAT- MEDLINE DA - 20101014 DCOM- 20101110 IS - 1791-7530 (Electronic) IS - 0250-7005 (Linking) VI - 30 IP - 9 DP - 2010 Sep TI - Sporadic breast carcinomas with somatic BRCA1 gene deletions share genotype/phenotype features with familial breast carcinomas. PG - 3445-9 AB - BACKGROUND: High frequencies of loss of heterozygosity (LOH) are found in familial breast carcinomas with BRCA mutations. Although LOH of BRCA1 does not coincide with somatic BRCA1 mutations, reduced BRCA1 protein expression and hypermethylation indicate the involvement of BRCA1 in sporadic carcinogenesis. To further investigate the role of BRCA we determined LOH of BRCA1 and correlated this with LOH in other breast cancer-associated regions. MATERIALS AND METHODS: A total of 105 sporadic breast carcinomas were analysed for LOH in the regions of BRCA1, BRCA2, TP53, Caveolin1, "putative BRCA3", PTEN, ATM and E-cadherin and correlated it with clinicopathological features. RESULTS: We found an overall increase of LOH in carcinomas with simultaneous LOH of BRCA1. Significantly higher LOH rates were detected in the regions of TP53 (80%: 34.7%; p<0.005), 8q21 (72.7%: 30.6%; p<0.010) and 10q22-23 (21.1%: 5.9%; p=0.043). Moreover, estrogen receptor-negative carcinomas revealed LOH of BRCA1 more frequently than estrogen receptor-positive carcinomas (39%: 12%; p=0.003). CONCLUSION: These data indicate that LOH of BRCA1 coincides with a defect of the DNA repair pathway. Therefore, LOH of BRCA1 determines a subgroup of sporadic breast carcinomas sharing genotype/phenotype features with familial breast carcinomas. AD - Department of Obstetrics and Gynecology, University of Cologne School of Medicine, Kerpener Str 34, 50931 Cologne, Germany. FAU - Rhiem, Kerstin AU - Rhiem K FAU - Todt, Unda AU - Todt U FAU - Wappenschmidt, Barbara AU - Wappenschmidt B FAU - Klein, Annette AU - Klein A FAU - Wardelmann, Eva AU - Wardelmann E FAU - Schmutzler, Rita K AU - Schmutzler RK LA - eng PT - Journal Article PL - Greece TA - Anticancer Res JT - Anticancer research JID - 8102988 RN - 0 (Cadherins) RN - 0 (Caveolin 1) RN - 0 (Cell Cycle Proteins) RN - 0 (DNA-Binding Proteins) RN - 0 (Tumor Markers, Biological) RN - 0 (Tumor Suppressor Proteins) RN - EC 2.7.1.37 (ataxia telangiectasia mutated protein) RN - EC 2.7.11.1 (Protein-Serine-Threonine Kinases) RN - EC 3.1.3.67 (PTEN Phosphohydrolase) SB - IM MH - Breast Neoplasms/*genetics/pathology MH - Cadherins/genetics MH - Caveolin 1/genetics MH - Cell Cycle Proteins/genetics MH - DNA-Binding Proteins/genetics MH - Female MH - *Gene Deletion MH - Gene Expression MH - Gene Expression Profiling MH - *Genes, BRCA1 MH - Genes, BRCA2 MH - Genes, p53 MH - Genetic Predisposition to Disease/genetics MH - Genotype MH - Humans MH - Loss of Heterozygosity MH - Neoplasm Staging MH - PTEN Phosphohydrolase/genetics MH - Phenotype MH - Polymerase Chain Reaction MH - Protein-Serine-Threonine Kinases/genetics MH - Tumor Markers, Biological/*genetics MH - Tumor Suppressor Proteins/genetics EDAT- 2010/10/15 06:00 MHDA- 2010/11/11 06:00 CRDT- 2010/10/15 06:00 AID - 30/9/3445 [pii] PST - ppublish SO - Anticancer Res. 2010 Sep;30(9):3445-9. PMID- 20944102 OWN - NLM STAT- MEDLINE DA - 20101014 DCOM- 20101110 IS - 1791-7530 (Electronic) IS - 0250-7005 (Linking) VI - 30 IP - 9 DP - 2010 Sep TI - Evidence for a tumour suppressor function of SETD2 in human breast cancer: a new hypothesis. PG - 3309-11 AB - BACKGROUND: SET domain containing protein 2 (SETD2) is a histone methyltransferase that is involved in transcriptional elongation. We previously demonstrated SETD2 to be a potential tumour suppressor gene in breast cancer. The aim of this study was to compare SETD2 expression in breast cancer with that in adjacent non-cancerous breast tissue (ANCT) in paired samples. A hypothesis is proposed that explains the mode of action of SETD2 as a tumour suppressor gene. MATERIALS AND METHODS: Paired samples of tumour and adjacent non-cancerous tissue (ANCT) from 25 patients were analysed. The levels of transcription of SETD2 were determined using quantitative polymerase chain reaction and normalized against cytokeratin 19. Immunohistochemical staining with appropriate antibodies against SETD2 protein was also performed in selected samples. RESULTS: Levels of SETD2 mRNA were significantly higher in ANCT when compared to those in tumour samples (p=0.01). Immunohistochemistry also demonstrated a higher protein expression in ANCT. CONCLUSION: This study offers further evidence that SETD2 behaves like a tumour suppressor gene. Our hypothesis links SETD2 mode of action with telomerase regulation through human telomerase reverse transcriptase (hTERT). Several studies have emphasised the importance of histone methylation of hTERT promotor in telomerase regulation. SETD2 function of histone methylation could be the missing link in this chain which could explain the potential tumour suppressor function of SETD2. AD - The Brunel Institute of Cancer Genetics and Pharmacogenomics, Brunel University, Uxbridge, Middlesex UB8 3PH, UK. FAU - Newbold, R F AU - Newbold RF FAU - Mokbel, K AU - Mokbel K LA - eng PT - Journal Article PL - Greece TA - Anticancer Res JT - Anticancer research JID - 8102988 RN - EC 2.1.1.43 (Histone-Lysine N-Methyltransferase) RN - EC 2.1.1.43 (Set2 protein, human) SB - IM MH - Breast Neoplasms/*genetics/metabolism MH - Female MH - Gene Expression MH - Gene Expression Profiling MH - *Genes, Tumor Suppressor MH - Histone-Lysine N-Methyltransferase/biosynthesis/*genetics MH - Humans MH - Immunohistochemistry MH - Reverse Transcriptase Polymerase Chain Reaction EDAT- 2010/10/15 06:00 MHDA- 2010/11/11 06:00 CRDT- 2010/10/15 06:00 AID - 30/9/3309 [pii] PST - ppublish SO - Anticancer Res. 2010 Sep;30(9):3309-11. PMID- 20939434 OWN - NLM STAT- MEDLINE DA - 20101013 DCOM- 20101026 IS - 0965-0407 (Print) IS - 0965-0407 (Linking) VI - 18 IP - 11-12 DP - 2010 TI - Association between the Thr431Asn polymorphism of the ROCK2 gene and risk of developing metastases of breast cancer. PG - 583-91 AB - The objective of this study was to analyze the genotype distributions and allele frequencies for ROCK2 Thr431Asn and Arg83Lys polymorphisms among breast cancer patients. In this case-control study, 223 patients with breast cancer were recruited and divided into two groups according to metastases (n = 128) and without metastases (n = 95). Genomic DNA from the patients and the control cases (n = 150) was analyzed by real-time PCR using a Light-Cycler. Neither genotype distributions nor the allele frequencies for the Arg83Lys polymorphism showed a significant difference between the groups. Although no marked changes were observed with nonmetastatic group, a statistically significant association was found between the control and metastatic group for the Thr431Asn polymorphism. Although homozygous carriers of the Thr431Thr genotype were more frequent, heterozygous carriers of the Thr431Asn genotype were less frequent among the metastatic patients than among controls. There was also an increase in Thr431 allele (60.5% in patients vs. 51.7% in controls) and decrease in Asn431 allele frequencies (48.3% in control vs. 39.5% in metastatic patients) in metastatic groups (p = 0.036). Our results demonstrate that Thr431Asn polymorphism of the ROCK2 gene could be a risk factor for the metastases of the breast cancer, and may help in predicting the prognosis. AD - Department of Medical Oncology, Faculty of Medicine, University of Gaziantep, Gaziantep, Turkey. FAU - Kalender, Mehmet E AU - Kalender ME FAU - Demiryurek, Seniz AU - Demiryurek S FAU - Oztuzcu, Serdar AU - Oztuzcu S FAU - Kizilyer, Ayse AU - Kizilyer A FAU - Demiryurek, Abdullah T AU - Demiryurek AT FAU - Sevinc, Alper AU - Sevinc A FAU - Dikilitas, Mustafa AU - Dikilitas M FAU - Yildiz, Ramazan AU - Yildiz R FAU - Camci, Celalettin AU - Camci C LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Oncol Res JT - Oncology research JID - 9208097 RN - 0 (ROCK2 protein, human) RN - EC 2.7.11.1 (rho-Associated Kinases) SB - IM MH - Adult MH - Aged MH - Breast Neoplasms/etiology/*genetics/pathology MH - Case-Control Studies MH - Female MH - Genotype MH - Humans MH - Middle Aged MH - Neoplasm Metastasis MH - *Polymorphism, Genetic MH - Risk Factors MH - rho-Associated Kinases/*genetics EDAT- 2010/10/14 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/10/14 06:00 PST - ppublish SO - Oncol Res. 2010;18(11-12):583-91. PMID- 20935267 OWN - NLM STAT- MEDLINE DA - 20101020 DCOM- 20101102 IS - 1460-2105 (Electronic) IS - 0027-8874 (Linking) VI - 102 IP - 20 DP - 2010 Oct 20 TI - StatBite: BRCA mutations in breast cancer patients under age 50 tested for mutations. PG - 1530 LA - eng PT - Journal Article DEP - 20101008 PL - United States TA - J Natl Cancer Inst JT - Journal of the National Cancer Institute JID - 7503089 SB - IM MH - Adult MH - Age Factors MH - Breast Neoplasms/*genetics MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Humans MH - Jews/*genetics MH - Middle Aged MH - *Mutation MH - Ovarian Neoplasms/genetics MH - Pedigree MH - Prevalence EDAT- 2010/10/12 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/10/12 06:00 PHST- 2010/10/08 [aheadofprint] AID - djq420 [pii] AID - 10.1093/jnci/djq420 [doi] PST - ppublish SO - J Natl Cancer Inst. 2010 Oct 20;102(20):1530. Epub 2010 Oct 8. PMID- 20924225 OWN - NLM STAT- MEDLINE DA - 20101006 DCOM- 20101102 IS - 1537-453X (Electronic) IS - 0277-3732 (Linking) VI - 33 IP - 5 DP - 2010 Oct TI - Breast conservation therapy in patients with stage T1-T2 breast cancer: current challenges and opportunities. PG - 500-10 AB - OBJECTIVES: Despite the fact that breast conservation therapy has been established as an effective treatment, a number of issues and controversies currently surround the application of this treatment for patients with stage T1 and T2 breast cancer. METHODS: Records of patients with histologically confirmed stage T1 (n = 1172) and stage T2 (n = 349) breast cancer, treated with wide local tumor excision and whole breast irradiation between January 1970 and December 2000, were prospectively registered on our database. Median follow-up was 6.6 years. Numerous publications addressing issues to be reviewed were collected, and data and prevailing controversies are discussed. RESULTS: The 10-year actuarial incidence of ipsilateral breast relapse was 7% for T1 and 11% for T2 tumors. Results with breast conservation therapy were equivalent in white or black women with T1 or T2 tumors. In patients younger than 40 years, incidence of failures was 10% for T1 (in contrast to 4% for other age groups) and 15% for T2 lesions (in contrast to 6% in other groups). The incidence of ipsilateral recurrences in women younger than 40 years was, for T1 tumors, 9% with negative surgical margins and 12% with close or positive margins and for T2 tumors 12% and 22%, respectively (difference not statistically significant). CONCLUSIONS: Use of breast-conserving surgical therapy should be optimized to enhance therapeutic outcome. Many developments in the oncological field and refinements in treatment planning and delivery of radiation therapy provide unique opportunities for the radiation oncologist to continue to play an integral role in the management of patients with breast cancer. AD - Department of Radiation Oncology, Siteman Cancer Center, Mallinckrodt Institute of Radiology, Washington University, St. Louis, MO, USA. cperez@radonc.wustl.edu FAU - Perez, Carlos A AU - Perez CA LA - eng PT - Journal Article PL - United States TA - Am J Clin Oncol JT - American journal of clinical oncology JID - 8207754 SB - IM MH - Adult MH - African Americans MH - Breast Neoplasms/ethnology/pathology/*radiotherapy/*surgery MH - Chemotherapy, Adjuvant MH - European Continental Ancestry Group MH - Female MH - Follow-Up Studies MH - Humans MH - *Mastectomy, Segmental MH - Missouri MH - Neoplasm Recurrence, Local MH - Proportional Hazards Models MH - Radiotherapy, Adjuvant MH - Survival Analysis MH - Treatment Outcome EDAT- 2010/10/07 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/10/07 06:00 AID - 10.1097/COC.0b013e3181d31f15 [doi] AID - 00000421-201010000-00014 [pii] PST - ppublish SO - Am J Clin Oncol. 2010 Oct;33(5):500-10. PMID- 20921543 OWN - NLM STAT- MEDLINE DA - 20101005 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 153 IP - 7 DP - 2010 Oct 5 TI - Screening and surveillance for second malignant neoplasms in adult survivors of childhood cancer: a report from the childhood cancer survivor study. PG - 442-51 AB - BACKGROUND: Survivors of childhood cancer may develop a second malignant neoplasm during adulthood and therefore require regular surveillance. OBJECTIVE: To examine adherence to population cancer screening guidelines by survivors at average risk for a second malignant neoplasm and adherence to cancer surveillance guidelines by survivors at high risk for a second malignant neoplasm. DESIGN: Retrospective cohort study. SETTING: The Childhood Cancer Survivor Study (CCSS), a 26-center study of long-term survivors of childhood cancer that was diagnosed between 1970 and 1986. PATIENTS: 4329 male and 4018 female survivors of childhood cancer who completed a CCSS questionnaire assessing screening and surveillance for new cases of cancer. MEASUREMENTS: Patient-reported receipt and timing of mammography, Papanicolaou smear, colonoscopy, or skin examination was categorized as adherent to the U.S. Preventive Services Task Force guidelines for survivors at average risk for breast or cervical cancer or the Children's Oncology Group guidelines for survivors at high risk for breast, colorectal, or skin cancer as a result of cancer therapy. RESULTS: In average-risk female survivors, 2743 of 3392 (80.9%) reported having a Papanicolaou smear within the recommended period, and 140 of 209 (67.0%) reported mammography within the recommended period. In high-risk survivors, rates of recommended mammography among women were only 241 of 522 (46.2%) and the rates of colonoscopy and complete skin examinations among both sexes were 91 of 794 (11.5%) and 1290 of 4850 (26.6%), respectively. LIMITATIONS: Data were self-reported. Participants in the CCSS are a selected group of survivors, and their adherence may not be representative of all survivors of childhood cancer. CONCLUSION: Female survivors at average risk for a second malignant neoplasm show reasonable rates of screening for cervical and breast cancer. However, surveillance for new cases of cancer is very low in survivors at the highest risk for colon, breast, or skin cancer, suggesting that survivors and their physicians need education about their risks and recommended surveillance. PRIMARY FUNDING SOURCE: The National Cancer Institute, National Institutes of Health, and the American Lebanese Syrian Associated Charities. AD - Hospital for Sick Children, Toronto, Ontario, Canada, USA. paul.nathan@sickkids.ca FAU - Nathan, Paul Craig AU - Nathan PC FAU - Ness, Kirsten Kimberlie AU - Ness KK FAU - Mahoney, Martin Christopher AU - Mahoney MC FAU - Li, Zhenghong AU - Li Z FAU - Hudson, Melissa Maria AU - Hudson MM FAU - Ford, Jennifer Sylene AU - Ford JS FAU - Landier, Wendy AU - Landier W FAU - Stovall, Marilyn AU - Stovall M FAU - Armstrong, Gregory Thomas AU - Armstrong GT FAU - Henderson, Tara Olive AU - Henderson TO FAU - Robison, Leslie L AU - Robison LL FAU - Oeffinger, Kevin Charles AU - Oeffinger KC LA - eng GR - U24-CA-55727/CA/NCI NIH HHS/United States PT - Journal Article PT - Multicenter Study PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 SB - AIM SB - IM SPIN- Ann Intern Med. 2010 Oct 5;153(7):I42. PMID: 20921538 MH - Adolescent MH - Adult MH - Breast Neoplasms/prevention & control MH - Child MH - Colorectal Neoplasms/prevention & control MH - Female MH - Humans MH - Male MH - *Mass Screening MH - Melanoma/prevention & control MH - Neoplasms, Second Primary/*prevention & control MH - *Patient Compliance MH - Retrospective Studies MH - Risk Factors MH - Skin Neoplasms/prevention & control MH - *Survivors MH - Young Adult EDAT- 2010/10/06 06:00 MHDA- 2010/11/17 06:00 CRDT- 2010/10/06 06:00 AID - 153/7/442 [pii] AID - 10.1059/0003-4819-153-7-201010050-00007 [doi] PST - ppublish SO - Ann Intern Med. 2010 Oct 5;153(7):442-51. PMID- 20886213 OWN - NLM STAT- MEDLINE DA - 20101018 DCOM- 20101029 LR - 20101104 IS - 1432-0843 (Electronic) IS - 0344-5704 (Linking) VI - 66 IP - 6 DP - 2010 Nov TI - Optimizing ixabepilone treatment schedules in patients with advanced or metastatic breast cancer. PG - 1005-12 AB - The epothilone B analog, ixabepilone, demonstrates low susceptibility to drug resistance mechanisms and has demonstrated clinically meaningful efficacy in patients refractory to other chemotherapeutic options. Ixabepilone is approved by the FDA for treatment of patients with metastatic breast cancer (MBC) progressing after taxanes and anthracyclines, either in combination with capecitabine or as monotherapy if the patient has already progressed on capecitabine. Ixabepilone is generally well tolerated at the approved dose and administration schedule of 40 mg/m(2) every 3 weeks. The most commonly observed dose-limiting adverse events (AEs) associated with ixabepilone are myelosuppression and peripheral neuropathy. Dose modification including dose reduction and dosing schedule modification may be utilized to manage toxicities, but this must be based on careful hematologic, neurologic, and liver function monitoring. Other ixabepilone dose schedules are being evaluated to further improve the risk/benefit profile. Weekly and daily schedules of ixabepilone have shown useful efficacy and reasonable tolerability. A recent phase II trial compared the tolerability of ixabepilone dosed once weekly (16 mg/m(2) on Days 1, 8, and 15 of each 28-day cycle) or every 3 weeks (40 mg/m(2) on Day 1 of each 21-day cycle) in patients with MBC. Preliminary data showed that both dosing schedules had an acceptable safety profile; however, more AEs were reported in patients receiving ixabepilone every 3 weeks. Ixabepilone is also being evaluated in combination with other anticancer agents (e.g., bevacizumab and lapatinib), in earlier breast cancer settings and in other indications. AD - Pharmacy Services, New York Oncology Hematology, 400 Patroon Creek Blvd, Ste 1, Albany, NY 12206, USA. Nancy.Egerton@usoncology.com FAU - Egerton, Nancy AU - Egerton N LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20101001 PL - Germany TA - Cancer Chemother Pharmacol JT - Cancer chemotherapy and pharmacology JID - 7806519 RN - 0 (Antibodies, Monoclonal) RN - 0 (Antineoplastic Agents) RN - 0 (Epothilones) RN - 0 (Quinazolines) RN - 0 (Tubulin Modulators) RN - 0 (bevacizumab) RN - 0 (epothilone B) RN - 0 (lapatinib) RN - 154361-50-9 (capecitabine) RN - 219989-84-1 (ixabepilone) RN - 51-21-8 (Fluorouracil) RN - 951-77-9 (Deoxycytidine) SB - IM MH - Antibodies, Monoclonal/administration & dosage MH - Antineoplastic Agents/*administration & dosage/adverse effects MH - Antineoplastic Combined Chemotherapy Protocols/therapeutic use MH - Bone Marrow/drug effects MH - Breast Neoplasms/*drug therapy/*pathology MH - Clinical Trials, Phase II as Topic MH - Deoxycytidine/administration & dosage/analogs & derivatives MH - Disease Progression MH - Drug Administration Schedule MH - Drug Interactions MH - Epothilones/*administration & dosage/adverse effects/chemistry MH - Female MH - Fluorouracil/administration & dosage/analogs & derivatives MH - Gene Expression Regulation, Neoplastic/drug effects MH - Humans MH - Lymphatic Metastasis MH - Peripheral Nervous System Diseases/chemically induced MH - Quinazolines/administration & dosage MH - Treatment Failure MH - Treatment Outcome MH - Tubulin Modulators/*administration & dosage/adverse effects PMC - PMC2955910 OID - NLM: PMC2955910 EDAT- 2010/10/05 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/10/02 06:00 PHST- 2010/05/17 [received] PHST- 2010/09/09 [accepted] PHST- 2010/10/01 [aheadofprint] AID - 10.1007/s00280-010-1467-x [doi] PST - ppublish SO - Cancer Chemother Pharmacol. 2010 Nov;66(6):1005-12. Epub 2010 Oct 1. PMID- 20877337 OWN - NLM STAT- MEDLINE DA - 20100929 DCOM- 20101025 LR - 20101102 IS - 1532-1827 (Electronic) IS - 0007-0920 (Linking) VI - 103 IP - 7 DP - 2010 Sep 28 TI - Increased cancer risks for relatives of very early-onset breast cancer cases with and without BRCA1 and BRCA2 mutations. PG - 1103-8 AB - BACKGROUND: Little is known regarding cancer risks for relatives of women with very early-onset breast cancer. METHODS: We studied 2208 parents and siblings of 504 unselected population-based Caucasian women with breast cancer diagnosed before age 35 years (103 from USA, 124 from Canada and 277 from Australia), 41 known to carry a mutation (24 in BRCA1, 16 in BRCA2 and one in both genes). Cancer-specific standardised incidence ratios (SIRs) were estimated by comparing the number of affected relatives (50% verified overall) with that expected based on incidences specific for country, sex, age and year of birth. RESULTS: For relatives of carriers, the female breast cancer SIRs were 13.13 (95% CI 6.57-26.26) and 12.52 (5.21-30.07) for BRCA1 and BRCA2, respectively. The ovarian cancer SIR was 12.38 (3.1-49.51) for BRCA1 and the prostate cancer SIR was 18.55 (4.64-74.17) for BRCA2. For relatives of non-carriers, the SIRs for female breast, prostate, lung, brain and urinary cancers were 4.03 (2.91-5.93), 5.25 (2.50-11.01), 7.73 (4.74-12.62), 5.19 (2.33-11.54) and 4.35 (1.81-10.46), respectively. For non-carriers, the SIRs remained elevated and were statistically significant for breast and prostate cancer when based on verified cancers. CONCLUSION: First-degree relatives of women with very early-onset breast cancer are at increased risk of cancers not explained by BRCA1 and BRCA2 mutations. AD - Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne, Level 1, 723 Swanston Street, Melbourne, Carlton VIC 3053, Australia. FAU - Dite, G S AU - Dite GS FAU - Whittemore, A S AU - Whittemore AS FAU - Knight, J A AU - Knight JA FAU - John, E M AU - John EM FAU - Milne, R L AU - Milne RL FAU - Andrulis, I L AU - Andrulis IL FAU - Southey, M C AU - Southey MC FAU - McCredie, M R E AU - McCredie MR FAU - Giles, G G AU - Giles GG FAU - Miron, A AU - Miron A FAU - Phipps, A I AU - Phipps AI FAU - West, D W AU - West DW FAU - Hopper, J L AU - Hopper JL LA - eng GR - CA-06-503/CA/NCI NIH HHS/United States GR - U01 CA69398/CA/NCI NIH HHS/United States GR - U01 CA69417/CA/NCI NIH HHS/United States GR - U01 CA69446/CA/NCI NIH HHS/United States GR - U01 CA69467/CA/NCI NIH HHS/United States GR - U01 CA69631/CA/NCI NIH HHS/United States GR - U01 CA69638/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100907 PL - England TA - Br J Cancer JT - British journal of cancer JID - 0370635 SB - IM MH - Adult MH - *Age of Onset MH - Breast Neoplasms/epidemiology/*genetics MH - *Family MH - Family Health MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Humans MH - Mothers MH - *Mutation MH - Risk MH - Siblings PMC - PMC2965877 OID - NLM: PMC2965877 [Available on 09/28/11] EDAT- 2010/09/30 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/09/30 06:00 PMCR- 2011/09/28 PHST- 2010/09/07 [aheadofprint] AID - 6605876 [pii] AID - 10.1038/sj.bjc.6605876 [doi] PST - ppublish SO - Br J Cancer. 2010 Sep 28;103(7):1103-8. Epub 2010 Sep 7. PMID- 20876427 OWN - NLM STAT- MEDLINE DA - 20101029 DCOM- 20101109 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 31 DP - 2010 Nov 1 TI - New pharmacogenomic paradigm in breast cancer treatment. PG - 4665-6 FAU - Offit, Kenneth AU - Offit K FAU - Robson, Mark E AU - Robson ME LA - eng PT - Comment PT - Editorial DEP - 20100927 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Antineoplastic Agents) RN - 0 (Aromatase Inhibitors) RN - 0 (Estrogens) RN - 0 (Proto-Oncogene Proteins) RN - 0 (TCL1A protein, human) SB - IM CON - J Clin Oncol. 2010 Nov 1;28(31):4674-82. PMID: 20876420 MH - Antineoplastic Agents/administration & dosage/*adverse effects MH - Aromatase Inhibitors/administration & dosage/*adverse effects MH - Breast Neoplasms/*drug therapy/*genetics/metabolism MH - Estrogens/*metabolism MH - Female MH - Humans MH - Odds Ratio MH - Pharmacogenetics MH - *Polymorphism, Single Nucleotide MH - Proto-Oncogene Proteins/*genetics MH - Research Design EDAT- 2010/09/30 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/09/30 06:00 PHST- 2010/09/27 [aheadofprint] AID - JCO.2010.31.2926 [pii] AID - 10.1200/JCO.2010.31.2926 [doi] PST - ppublish SO - J Clin Oncol. 2010 Nov 1;28(31):4665-6. Epub 2010 Sep 27. PMID- 20876420 OWN - NLM STAT- MEDLINE DA - 20101029 DCOM- 20101109 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 31 DP - 2010 Nov 1 TI - Genome-wide associations and functional genomic studies of musculoskeletal adverse events in women receiving aromatase inhibitors. PG - 4674-82 AB - PURPOSE: We performed a case-control genome-wide association study (GWAS) to identify single nucleotide polymorphisms (SNPs) associated with musculoskeletal adverse events (MS-AEs) in women treated with aromatase inhibitors (AIs) for early breast cancer. PATIENTS AND METHODS: A nested case-control design was used to select patients enrolled onto the MA.27 phase III trial comparing anastrozole with exemestane. Cases were matched to two controls and were defined as patients with grade 3 or 4 MS-AEs (according to the National Cancer Institute's Common Terminology Criteria for Adverse Events v3.0) or those who discontinued treatment for any grade of MS-AE within the first 2 years. Genotyping was performed with the Illumina Human610-Quad BeadChip. RESULTS: The GWAS included 293 cases and 585 controls. A total of 551,358 SNPs were analyzed, followed by imputation and fine mapping of a region of interest on chromosome 14. Four SNPs on chromosome 14 had the lowest P values (2.23E-06 to 6.67E-07). T-cell leukemia 1A (TCL1A) was the gene closest (926-7000 bp) to the four SNPs. Functional genomic studies revealed that one of these SNPs (rs11849538) created an estrogen response element and that TCL1A expression was estrogen dependent, was associated with the variant SNP genotypes in estradiol-treated lymphoblastoid cells transfected with estrogen receptor alpha and was directly related to interleukin 17 receptor A (IL17RA) expression. CONCLUSION: This GWAS identified SNPs associated with MS-AEs in women treated with AIs and with a gene (TCL1A) which, in turn, was related to a cytokine (IL17). These findings provide a focus for further research to identify patients at risk for MS-AEs and to explore the mechanisms for these adverse events. AD - Mayo Clinic, Rochester, MN 55905, USA. ingle.james@mayo.edu FAU - Ingle, James N AU - Ingle JN FAU - Schaid, Daniel J AU - Schaid DJ FAU - Goss, Paul E AU - Goss PE FAU - Liu, Mohan AU - Liu M FAU - Mushiroda, Taisei AU - Mushiroda T FAU - Chapman, Judy-Anne W AU - Chapman JA FAU - Kubo, Michiaki AU - Kubo M FAU - Jenkins, Gregory D AU - Jenkins GD FAU - Batzler, Anthony AU - Batzler A FAU - Shepherd, Lois AU - Shepherd L FAU - Pater, Joseph AU - Pater J FAU - Wang, Liewei AU - Wang L FAU - Ellis, Matthew J AU - Ellis MJ FAU - Stearns, Vered AU - Stearns V FAU - Rohrer, Daniel C AU - Rohrer DC FAU - Goetz, Matthew P AU - Goetz MP FAU - Pritchard, Kathleen I AU - Pritchard KI FAU - Flockhart, David A AU - Flockhart DA FAU - Nakamura, Yusuke AU - Nakamura Y FAU - Weinshilboum, Richard M AU - Weinshilboum RM LA - eng GR - P50CA116201/CA/NCI NIH HHS/United States GR - U01GM61388/GM/NIGMS NIH HHS/United States GR - U01GM63173/GM/NIGMS NIH HHS/United States GR - U10CA77202/CA/NCI NIH HHS/United States PT - Comparative Study PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100927 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Androstadienes) RN - 0 (Antineoplastic Agents) RN - 0 (Aromatase Inhibitors) RN - 0 (Estrogens) RN - 0 (IL17RA protein, human) RN - 0 (Nitriles) RN - 0 (Proto-Oncogene Proteins) RN - 0 (Receptors, Interleukin-17) RN - 0 (TCL1A protein, human) RN - 0 (Triazoles) RN - 107868-30-4 (exemestane) RN - 120511-73-1 (anastrozole) SB - IM CIN - J Clin Oncol. 2010 Nov 1;28(31):4665-6. PMID: 20876427 MH - Aged MH - Aged, 80 and over MH - Androstadienes/adverse effects MH - Antineoplastic Agents/administration & dosage/*adverse effects MH - Aromatase Inhibitors/administration & dosage/*adverse effects MH - Breast Neoplasms/*drug therapy/genetics/metabolism/pathology MH - Case-Control Studies MH - Chromosome Mapping MH - *Chromosomes, Human, Pair 14 MH - Clinical Trials, Phase III as Topic MH - Estrogens/metabolism MH - Female MH - Gene Expression Regulation, Neoplastic MH - Genome-Wide Association Study MH - Genotype MH - Humans MH - Logistic Models MH - Middle Aged MH - Musculoskeletal System/*drug effects MH - Neoplasm Staging MH - Nitriles/adverse effects MH - *Polymorphism, Single Nucleotide MH - Postmenopause MH - Proto-Oncogene Proteins/*genetics MH - Randomized Controlled Trials as Topic MH - Receptors, Interleukin-17/*metabolism MH - Retrospective Studies MH - Severity of Illness Index MH - Triazoles/adverse effects EDAT- 2010/09/30 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/09/30 06:00 PHST- 2010/09/27 [aheadofprint] AID - JCO.2010.28.5064 [pii] AID - 10.1200/JCO.2010.28.5064 [doi] PST - ppublish SO - J Clin Oncol. 2010 Nov 1;28(31):4674-82. Epub 2010 Sep 27. PMID- 20871616 OWN - NLM STAT- MEDLINE DA - 20101006 DCOM- 20101116 IS - 1545-9985 (Electronic) IS - 1545-9985 (Linking) VI - 17 IP - 10 DP - 2010 Oct TI - Enhancement of RAD51 recombinase activity by the tumor suppressor PALB2. PG - 1255-9 AB - Homologous recombination mediated by RAD51 recombinase helps eliminate chromosomal lesions, such as DNA double-strand breaks induced by radiation or arising from injured DNA replication forks. The tumor suppressors BRCA2 and PALB2 act together to deliver RAD51 to chromosomal lesions to initiate repair. Here we document a new function of PALB2: to enhance RAD51's ability to form the D loop. We show that PALB2 binds DNA and physically interacts with RAD51. Notably, although PALB2 alone stimulates D-loop formation, it has a cooperative effect with RAD51AP1, an enhancer of RAD51. This stimulation stems from the ability of PALB2 to function with RAD51 and RAD51AP1 to assemble the synaptic complex. Our results demonstrate the multifaceted role of PALB2 in chromosome damage repair. Because PALB2 mutations can cause cancer or Fanconi anemia, our findings shed light on the mechanism of tumor suppression in humans. AD - Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, Connecticut, USA. eloise.dray@yale.edu FAU - Dray, Eloise AU - Dray E FAU - Etchin, Julia AU - Etchin J FAU - Wiese, Claudia AU - Wiese C FAU - Saro, Dorina AU - Saro D FAU - Williams, Gareth J AU - Williams GJ FAU - Hammel, Michal AU - Hammel M FAU - Yu, Xiong AU - Yu X FAU - Galkin, Vitold E AU - Galkin VE FAU - Liu, Dongqing AU - Liu D FAU - Tsai, Miaw-Sheue AU - Tsai MS FAU - Sy, Shirley M-H AU - Sy SM FAU - Schild, David AU - Schild D FAU - Egelman, Edward AU - Egelman E FAU - Chen, Junjie AU - Chen J FAU - Sung, Patrick AU - Sung P LA - eng GR - P01CA129186/CA/NCI NIH HHS/United States GR - P01CA92584/CA/NCI NIH HHS/United States GR - R01CA120315/CA/NCI NIH HHS/United States GR - R01ES015252/ES/NIEHS NIH HHS/United States GR - R01ES015632/ES/NIEHS NIH HHS/United States GR - R01ES07061/ES/NIEHS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100926 PL - United States TA - Nat Struct Mol Biol JT - Nature structural & molecular biology JID - 101186374 RN - 0 (BLID protein, human) RN - 0 (BRCA2 Protein) RN - 0 (DNA, Neoplasm) RN - 0 (DNA-Binding Proteins) RN - 0 (Multiprotein Complexes) RN - 0 (Neoplasm Proteins) RN - 0 (Nuclear Proteins) RN - 0 (PALB2 protein, human) RN - 0 (Peptide Fragments) RN - 0 (RAD51AP1 protein, human) RN - 0 (Recombinant Fusion Proteins) RN - 0 (Tumor Suppressor Proteins) RN - EC 2.7.7.- (RAD51 protein, human) RN - EC 2.7.7.- (Rad51 Recombinase) SB - IM MH - BRCA2 Protein/chemistry/*physiology MH - Breast Neoplasms/*metabolism MH - DNA Repair/*physiology MH - DNA, Neoplasm/*metabolism MH - DNA-Binding Proteins/chemistry/*physiology MH - Female MH - Humans MH - Multiprotein Complexes MH - Neoplasm Proteins/chemistry/*physiology MH - Nuclear Proteins/chemistry/genetics/*physiology MH - Peptide Fragments/metabolism MH - Protein Binding MH - Protein Interaction Mapping MH - Rad51 Recombinase/chemistry/*physiology MH - Recombinant Fusion Proteins/chemistry/physiology MH - Recombination, Genetic/*physiology MH - Tumor Suppressor Proteins/chemistry/genetics/*physiology PMC - PMC2950913 MID - NIHMS231461 OID - NLM: NIHMS231461 [Available on 04/01/11] OID - NLM: PMC2950913 [Available on 04/01/11] EDAT- 2010/09/28 06:00 MHDA- 2010/11/17 06:00 CRDT- 2010/09/28 06:00 PMCR- 2011/04/01 PHST- 2010/04/14 [received] PHST- 2010/08/24 [accepted] PHST- 2010/09/26 [aheadofprint] AID - nsmb.1916 [pii] AID - 10.1038/nsmb.1916 [doi] PST - ppublish SO - Nat Struct Mol Biol. 2010 Oct;17(10):1255-9. Epub 2010 Sep 26. PMID- 20871615 OWN - NLM STAT- MEDLINE DA - 20101006 DCOM- 20101116 IS - 1545-9985 (Electronic) IS - 1545-9985 (Linking) VI - 17 IP - 10 DP - 2010 Oct TI - Cooperation of breast cancer proteins PALB2 and piccolo BRCA2 in stimulating homologous recombination. PG - 1247-54 AB - Inherited mutations in human PALB2 are associated with a predisposition to breast and pancreatic cancers. PALB2's tumor-suppressing effect is thought to be based on its ability to facilitate BRCA2's function in homologous recombination. However, the biochemical properties of PALB2 are unknown. Here we show that human PALB2 binds DNA, preferentially D-loop structures, and directly interacts with the RAD51 recombinase to stimulate strand invasion, a vital step of homologous recombination. This stimulation occurs through reinforcing biochemical mechanisms, as PALB2 alleviates inhibition by RPA and stabilizes the RAD51 filament. Moreover, PALB2 can function synergistically with a BRCA2 chimera (termed piccolo, or piBRCA2) to further promote strand invasion. Finally, we show that PALB2-deficient cells are sensitive to PARP inhibitors. Our studies provide the first biochemical insights into PALB2's function with piBRCA2 as a mediator of homologous recombination in DNA double-strand break repair. AD - Genome Stability Laboratory, Laval University Cancer Research Center, Hotel-Dieu de Quebec, Quebec City, Quebec, Canada. FAU - Buisson, Remi AU - Buisson R FAU - Dion-Cote, Anne-Marie AU - Dion-Cote AM FAU - Coulombe, Yan AU - Coulombe Y FAU - Launay, Helene AU - Launay H FAU - Cai, Hong AU - Cai H FAU - Stasiak, Alicja Z AU - Stasiak AZ FAU - Stasiak, Andrzej AU - Stasiak A FAU - Xia, Bing AU - Xia B FAU - Masson, Jean-Yves AU - Masson JY LA - eng GR - R01CA138804/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100926 PL - United States TA - Nat Struct Mol Biol JT - Nature structural & molecular biology JID - 101186374 RN - 0 (BLID protein, human) RN - 0 (BRCA2 Protein) RN - 0 (DNA, Neoplasm) RN - 0 (Neoplasm Proteins) RN - 0 (Nuclear Proteins) RN - 0 (PALB2 protein, human) RN - 0 (Peptide Fragments) RN - 0 (Tumor Suppressor Proteins) RN - EC 2.4.2.30 (PARP1 protein, human) RN - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases) RN - EC 2.7.7.- (RAD51 protein, human) RN - EC 2.7.7.- (Rad51 Recombinase) SB - IM MH - BRCA2 Protein/chemistry/*physiology MH - Base Sequence MH - Breast Neoplasms/*metabolism MH - DNA Breaks, Double-Stranded MH - DNA Repair/*physiology MH - DNA, Neoplasm/*metabolism MH - Female MH - Humans MH - Models, Biological MH - Molecular Sequence Data MH - Neoplasm Proteins/chemistry/*physiology MH - Nuclear Proteins/chemistry/genetics/*physiology MH - Nucleic Acid Conformation MH - Peptide Fragments/chemistry/metabolism MH - Poly(ADP-ribose) Polymerases/antagonists & inhibitors MH - Protein Interaction Domains and Motifs MH - Protein Interaction Mapping MH - Rad51 Recombinase/chemistry/*physiology MH - Recombination, Genetic/*physiology MH - Structure-Activity Relationship MH - Tumor Suppressor Proteins/chemistry/genetics/*physiology EDAT- 2010/09/28 06:00 MHDA- 2010/11/17 06:00 CRDT- 2010/09/28 06:00 PHST- 2010/04/12 [received] PHST- 2010/08/16 [accepted] PHST- 2010/09/26 [aheadofprint] AID - nsmb.1915 [pii] AID - 10.1038/nsmb.1915 [doi] PST - ppublish SO - Nat Struct Mol Biol. 2010 Oct;17(10):1247-54. Epub 2010 Sep 26. PMID- 20864719 OWN - NLM STAT- MEDLINE DA - 20101011 DCOM- 20101025 IS - 1541-0048 (Electronic) IS - 0090-0036 (Linking) VI - 100 IP - 11 DP - 2010 Nov TI - Beyond recreational physical activity: examining occupational and household activity, transportation activity, and sedentary behavior in relation to postmenopausal breast cancer risk. PG - 2288-95 AB - OBJECTIVES: We prospectively examined nonrecreational physical activity and sedentary behavior in relation to breast cancer risk among 97 039 postmenopausal women in the National Institutes of Health-AARP Diet and Health Study. METHODS: We identified 2866 invasive and 570 in situ breast cancer cases recorded between 1996 and 2003 and used Cox proportional hazards regression to estimate multivariate relative risks (RRs) and 95% confidence intervals (CIs). RESULTS: Routine activity during the day at work or at home that included heavy lifting or carrying versus mostly sitting was associated with reduced risk of invasive breast cancer (RR = 0.62; 95% CI = 0.42, 0.91; P(trend) = .024). CONCLUSIONS: Routine activity during the day at work or home may be related to reduced invasive breast cancer risk. Domains outside of recreation time may be attractive targets for increasing physical activity and reducing sedentary behavior among postmenopausal women. AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA. materess@mail.nih.gov FAU - George, Stephanie M AU - George SM FAU - Irwin, Melinda L AU - Irwin ML FAU - Matthews, Charles E AU - Matthews CE FAU - Mayne, Susan T AU - Mayne ST FAU - Gail, Mitchell H AU - Gail MH FAU - Moore, Steven C AU - Moore SC FAU - Albanes, Demetrius AU - Albanes D FAU - Ballard-Barbash, Rachel AU - Ballard-Barbash R FAU - Hollenbeck, Albert R AU - Hollenbeck AR FAU - Schatzkin, Arthur AU - Schatzkin A FAU - Leitzmann, Michael F AU - Leitzmann MF LA - eng GR - T32 CA105666/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, N.I.H., Intramural DEP - 20100923 PL - United States TA - Am J Public Health JT - American journal of public health JID - 1254074 SB - AIM SB - IM MH - Age Factors MH - Breast Neoplasms/epidemiology/*etiology MH - Confidence Intervals MH - Exercise MH - Family Characteristics MH - Female MH - Humans MH - Middle Aged MH - *Motor Activity MH - Postmenopause MH - Proportional Hazards Models MH - Recreation MH - Risk MH - Risk Factors MH - *Sedentary Lifestyle MH - Time Factors MH - Transportation/statistics & numerical data MH - United States/epidemiology MH - Workplace/statistics & numerical data EDAT- 2010/09/25 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/09/25 06:00 PHST- 2010/09/23 [aheadofprint] AID - AJPH.2009.180828 [pii] AID - 10.2105/AJPH.2009.180828 [doi] PST - ppublish SO - Am J Public Health. 2010 Nov;100(11):2288-95. Epub 2010 Sep 23. PMID- 20858745 OWN - NLM STAT- MEDLINE DA - 20101011 DCOM- 20101102 IS - 1476-6256 (Electronic) IS - 0002-9262 (Linking) VI - 172 IP - 8 DP - 2010 Oct 15 TI - A population-based case-control study of fetal growth, gestational age, and maternal breast cancer. PG - 962-70 AB - Fetal growth or gestational age in a woman's pregnancies may modify pregnancy-related breast cancer risk, yet studies of these exposures are few. The authors conducted a population-based case-control study among parous Michigan women aged /=30 years modestly reduced risk: odds ratio = 0.82 (95% confidence interval: 0.68, 0.98). First delivery at <32 or >41 weeks also modestly reduced risk: odds ratio = 0.80 (95% confidence interval: 0.62, 1.04) or 0.92 (95% confidence interval: 0.85, 0.99), respectively. In the largest case-control study to date, fetal growth was not associated with overall breast cancer risk in women aged 2.7n) in 45% of the cases and an average nonaberrant cell admixture of 49%. By aggregation of ASCAT profiles across our series, we obtain genomic frequency distributions of gains and losses, as well as genome-wide views of LOH and copy number-neutral events in breast cancer. In addition, the ASCAT profiles reveal differences in aberrant tumor cell fraction, ploidy, gains, losses, LOH, and copy number-neutral events between the five previously identified molecular breast cancer subtypes. Basal-like breast carcinomas have a significantly higher frequency of LOH compared with other subtypes, and their ASCAT profiles show large-scale loss of genomic material during tumor development, followed by a whole-genome duplication, resulting in near-triploid genomes. Finally, from the ASCAT profiles, we construct a genome-wide map of allelic skewness in breast cancer, indicating loci where one allele is preferentially lost, whereas the other allele is preferentially gained. We hypothesize that these alternative alleles have a different influence on breast carcinoma development. AD - Department of Genetics, Institute for Cancer Research, Clinic for Cancer and Surgery, Oslo University Hospital, Montebello, N-0310 Oslo, Norway. FAU - Van Loo, Peter AU - Van Loo P FAU - Nordgard, Silje H AU - Nordgard SH FAU - Lingjaerde, Ole Christian AU - Lingjaerde OC FAU - Russnes, Hege G AU - Russnes HG FAU - Rye, Inga H AU - Rye IH FAU - Sun, Wei AU - Sun W FAU - Weigman, Victor J AU - Weigman VJ FAU - Marynen, Peter AU - Marynen P FAU - Zetterberg, Anders AU - Zetterberg A FAU - Naume, Bjorn AU - Naume B FAU - Perou, Charles M AU - Perou CM FAU - Borresen-Dale, Anne-Lise AU - Borresen-Dale AL FAU - Kristensen, Vessela N AU - Kristensen VN LA - eng GR - P50-CA58223-09A1/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100913 PL - United States TA - Proc Natl Acad Sci U S A JT - Proceedings of the National Academy of Sciences of the United States of America JID - 7505876 SB - IM MH - Alleles MH - Breast Neoplasms/*genetics MH - Carcinoma/*genetics MH - Female MH - *Gene Dosage MH - *Genes, Neoplasm MH - *Genome, Human MH - Humans MH - Ploidies PMC - PMC2947907 OID - NLM: PMC2947907 EDAT- 2010/09/15 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/09/15 06:00 PHST- 2010/09/13 [aheadofprint] AID - 1009843107 [pii] AID - 10.1073/pnas.1009843107 [doi] PST - ppublish SO - Proc Natl Acad Sci U S A. 2010 Sep 28;107(39):16910-5. Epub 2010 Sep 13. PMID- 20836941 OWN - NLM STAT- MEDLINE DA - 20100914 DCOM- 20101026 IS - 1479-1072 (Print) IS - 1479-1064 (Linking) VI - 18 IP - 4 DP - 2010 TI - A critical review of the literature on the uptake of cervical and breast screening in British South Asian women. PG - 251-61 AB - OBJECTIVES: To consider the recent evidence which examines factors that are associated with uptake of cervical and breast screening in the British South Asian community and to consider the effectiveness of interventions to improve uptake in this group. METHODS: A search strategy was developed and key databases were searched to identify primary research studies that examined the uptake of cervical and breast screening in British women of South Asian origin. Studies published prior to 1996 were excluded from the review. RESULTS: Seventy-eight studies were identified and ten were included in the review. Observational studies demonstrated mixed results on the effect of ethnicity on uptake of screening. Controlling for confounders attenuated the effect in all studies and removed its effect entirely in some. Investigation of low uptake in qualitative and quantitative research indicates that South Asian women were more likely to have incorrect addresses and language or cultural barriers to screening than other women. Few interventional studies were identified and all varied in their design. The success of interventions was mixed and the lack of control groups in some studies made it difficult to draw conclusions on their effectiveness. CONCLUSION: There is a poor uptake of cervical and breast screening by South Asian women compared with the general population in Britain. Evidence is inconclusive as to whether this is due to a residual effect of ethnicity following control for socio-demographic and local health service variables. Currently there is a lack of robust experimental studies on which to base interventions intended to increase uptake in this population. AD - NHS Nottinghamshire County, Nottinghamshire, UK. rachel.sokal@nhs.net FAU - Sokal, Rachel AU - Sokal R LA - eng PT - Journal Article PT - Review PL - England TA - Qual Prim Care JT - Quality in primary care JID - 101182136 SB - IM MH - Asia, Southeastern/ethnology MH - Breast Neoplasms/*diagnosis/*ethnology MH - Clinical Trials as Topic MH - Female MH - Great Britain/epidemiology MH - Health Services Accessibility/organization & administration MH - Humans MH - Mass Screening/*statistics & numerical data MH - Uterine Cervical Neoplasms/*diagnosis/*ethnology EDAT- 2010/09/15 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/09/15 06:00 PST - ppublish SO - Qual Prim Care. 2010;18(4):251-61. PMID- 20805458 OWN - NLM STAT- MEDLINE DA - 20101008 DCOM- 20101029 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 29 DP - 2010 Oct 10 TI - Alcohol consumption and breast cancer recurrence and survival among women with early-stage breast cancer: the life after cancer epidemiology study. PG - 4410-6 AB - PURPOSE: To examine the association of alcohol consumption after breast cancer diagnosis with recurrence and mortality among early-stage breast cancer survivors. PATIENTS AND METHODS: Patients included 1,897 LACE study participants diagnosed with early-stage breast cancer between 1997 and 2000 and recruited on average 2 years postdiagnosis, primarily from the Kaiser Permanente Northern California Cancer Registry. Alcohol consumption (ie, wine, beer, and liquor) was assessed at cohort entry using a food frequency questionnaire. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% CI with adjustment for known prognostic factors. RESULTS: Two hundred ninety-three breast cancer recurrences and 273 overall deaths were ascertained after an average follow-up of 7.4 years. Nine hundred fifty-eight women (51%) were considered drinkers (> 0.5 g/d of alcohol), and the majority drank wine (89%). Drinking >/= 6 g/d of alcohol compared with no drinking was associated with an increased risk of breast cancer recurrence (HR, 1.35; 95% CI, 1.00 to 1.83) and death due to breast cancer (HR, 1.51; 95% CI, 1.00 to 2.29). The increased risk of recurrence appeared to be greater among postmenopausal (HR, 1.51; 95% CI, 1.05 to 2.19) and overweight and obese women (HR, 1.60; 95% CI, 1.08 to 2.38). Alcohol intake was not associated with all-cause death and possibly associated with decreased risk of non-breast cancer death. CONCLUSION: Consuming three to four alcoholic drinks or more per week after a breast cancer diagnosis may increase risk of breast cancer recurrence, particularly among postmenopausal and overweight/obese women, yet the cardioprotective effects of alcohol on non-breast cancer death were suggested. AD - Division of Research, Kaiser Permanente, 2000 Oakland, CA 94612, USA. Marilyn.L.Kwan@kp.org FAU - Kwan, Marilyn L AU - Kwan ML FAU - Kushi, Lawrence H AU - Kushi LH FAU - Weltzien, Erin AU - Weltzien E FAU - Tam, Emily K AU - Tam EK FAU - Castillo, Adrienne AU - Castillo A FAU - Sweeney, Carol AU - Sweeney C FAU - Caan, Bette J AU - Caan BJ LA - eng GR - R01 CA129059/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20100830 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 SB - IM CIN - J Clin Oncol. 2010 Oct 10;28(29):4403-4. PMID: 20805447 MH - Adolescent MH - Adult MH - Aged MH - *Alcohol Drinking MH - Breast Neoplasms/*epidemiology/pathology MH - California/epidemiology MH - Female MH - Humans MH - Middle Aged MH - Neoplasm Recurrence, Local MH - Neoplasm Staging MH - Overweight MH - Postmenopause MH - Proportional Hazards Models MH - *Questionnaires MH - Risk Assessment/methods/statistics & numerical data MH - Risk Factors MH - Survival Analysis MH - Young Adult EDAT- 2010/09/02 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/09/01 06:00 PHST- 2010/08/30 [aheadofprint] AID - JCO.2010.29.2730 [pii] AID - 10.1200/JCO.2010.29.2730 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 10;28(29):4410-6. Epub 2010 Aug 30. PMID- 20805453 OWN - NLM STAT- MEDLINE DA - 20100930 DCOM- 20101102 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 28 DP - 2010 Oct 1 TI - Molecular anatomy of breast cancer stroma and its prognostic value in estrogen receptor-positive and -negative cancers. PG - 4316-23 AB - PURPOSE: The purpose of this study was to identify genes enriched in breast cancer stroma, assess the stromal gene expression differences between estrogen receptor (ER) -positive and -negative cancers, and separately determine their prognostic value in these two subtypes of breast cancers. METHODS: We compared gene expression profiles of pairs of fine-needle (stroma-poor) and core-needle (stroma-rich) biopsies from 37 cancers to identify stroma-associated genes. We defined stromal metagenes and tested their prognostic values in 684 node-negative patients who received no systemic adjuvant therapy and 259 tamoxifen-treated patients. RESULTS: We identified 293 probe sets overexpressed in core biopsies; these included five highly coexpressed gene clusters (metagenes) corresponding to immune functions and extracellular matrix components. These genes showed quantitative and qualitative differences between ER-positive and ER-negative cancers. A B-cell/plasma cell metagene showed strong prognostic value in ER-positive highly proliferative cancers, a lesser prognostic value in ER-negative cancers, and no prognostic value in ER-positive cancers with low proliferation. The hazard ratio for distant relapse in the lowest compared with the highest tertile of the pooled prognostic data set was 4.29 (95% CI, 2.04 to 9.01; P = .001) in ER-positive cancers and 3.34 (95% CI, 1.60 to 6.97; P = .001) in ER-negative cancers. This remained significant in multivariate analysis including routine variables and other genomic prognostic scores. As a result of quantitative differences in this metagene between ER-positive and ER-negative cancers, different thresholds apply in the two subgroups. Other stromal metagenes had inconsistent prognostic value. CONCLUSION: Among ER-negative and ER-positive highly proliferative cancers, a subset of tumors with high expression of a B-cell/plasma cell metagene carries a favorable prognosis. AD - Department of Breast Medical Oncology, Unit 1354, The University of Texas M. D. Anderson Cancer Center, PO Box 301439, Houston,TX 77230-1439, USA. FAU - Bianchini, Giampaolo AU - Bianchini G FAU - Qi, Yuan AU - Qi Y FAU - Alvarez, Ricardo H AU - Alvarez RH FAU - Iwamoto, Takayuki AU - Iwamoto T FAU - Coutant, Charles AU - Coutant C FAU - Ibrahim, Nuhad K AU - Ibrahim NK FAU - Valero, Vicente AU - Valero V FAU - Cristofanilli, Massimo AU - Cristofanilli M FAU - Green, Marjorie C AU - Green MC FAU - Radvanyi, Laszlo AU - Radvanyi L FAU - Hatzis, Christos AU - Hatzis C FAU - Hortobagyi, Gabriel N AU - Hortobagyi GN FAU - Andre, Fabrice AU - Andre F FAU - Gianni, Luca AU - Gianni L FAU - Symmans, W Fraser AU - Symmans WF FAU - Pusztai, Lajos AU - Pusztai L LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100830 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Amyloid beta-Protein Precursor) RN - 0 (Antineoplastic Agents, Hormonal) RN - 0 (COL4A2 protein, human) RN - 0 (Collagen Type IV) RN - 0 (ECM1 protein, human) RN - 0 (Extracellular Matrix Proteins) RN - 0 (PLTP protein, human) RN - 0 (Phospholipid Transfer Proteins) RN - 0 (Receptors, Cell Surface) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Transforming Growth Factor beta) RN - 0 (protease nexins) RN - 10540-29-1 (Tamoxifen) RN - EC 2.7.11.1 (Protein-Serine-Threonine Kinases) RN - EC 2.7.11.30 (transforming growth factor-beta type II receptor) SB - IM MH - Amyloid beta-Protein Precursor/genetics MH - Antineoplastic Agents, Hormonal/therapeutic use MH - B-Lymphocytes/pathology MH - Biopsy, Fine-Needle MH - Breast Neoplasms/drug therapy/*genetics/pathology MH - Chi-Square Distribution MH - Collagen Type IV/genetics MH - Extracellular Matrix Proteins MH - Female MH - Gene Expression Profiling MH - Gene Expression Regulation, Neoplastic MH - Humans MH - Metagenome/genetics MH - Neoplasm Recurrence, Local MH - Phospholipid Transfer Proteins/genetics MH - Prognosis MH - Proportional Hazards Models MH - Prospective Studies MH - Protein-Serine-Threonine Kinases/genetics MH - Receptors, Cell Surface/genetics MH - Receptors, Estrogen/*genetics MH - Receptors, Transforming Growth Factor beta/genetics MH - Survival Analysis MH - Tamoxifen/therapeutic use EDAT- 2010/09/02 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/09/01 06:00 PHST- 2010/08/30 [aheadofprint] AID - JCO.2009.27.2419 [pii] AID - 10.1200/JCO.2009.27.2419 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 1;28(28):4316-23. Epub 2010 Aug 30. PMID- 20805447 OWN - NLM STAT- MEDLINE DA - 20101008 DCOM- 20101029 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 29 DP - 2010 Oct 10 TI - Challenge of balancing alcohol intake. PG - 4403-4 FAU - Holmes, Michelle D AU - Holmes MD LA - eng PT - Comment PT - Editorial DEP - 20100830 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 SB - IM CON - J Clin Oncol. 2010 Oct 10;28(29):4410-6. PMID: 20805458 MH - *Alcohol Drinking MH - Breast Neoplasms/*epidemiology/pathology MH - Female MH - Humans MH - Neoplasm Recurrence, Local MH - Neoplasm Staging MH - Proportional Hazards Models MH - Risk Assessment/methods/statistics & numerical data MH - Risk Factors MH - Survival Analysis EDAT- 2010/09/02 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/09/01 06:00 PHST- 2010/08/30 [aheadofprint] AID - JCO.2010.31.0102 [pii] AID - 10.1200/JCO.2010.31.0102 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 10;28(29):4403-4. Epub 2010 Aug 30. PMID- 20736952 OWN - NLM STAT- MEDLINE DA - 20100929 DCOM- 20101025 LR - 20101102 IS - 1532-1827 (Electronic) IS - 0007-0920 (Linking) VI - 103 IP - 7 DP - 2010 Sep 28 TI - Combination of osteopontin and activated leukocyte cell adhesion molecule as potent prognostic discriminators in HER2- and ER-negative breast cancer. PG - 1048-56 AB - BACKGROUND: To analyse the discriminative impact of osteopontin (OPN) and activated leukocyte cell adhesion molecule (ALCAM), combined with human epidermal growth factor 2 (HER2) and oestrogen receptor (ER) in breast cancer. METHODS: Osteopontin, ALCAM, HER2 and ER mRNA expression in breast cancer tissues of 481 patients were analysed (mRNA microarray analysis, kinetic RT-PCR). Hierarchical clustering was performed in training cohort A (N=100, adjuvant treatment) and validation cohorts B (N=200, no adjuvant treatment, low-risk) and C (N=181, adjuvant treatment, high-risk). RESULTS: Negative/low ER and HER2, high OPN and low ALCAM mRNA expression helped to identify patients at particularly high risk, showing shorter DFS, P<0.001, and OAS, P=0.001. Although both validation cohorts showed diverse risk and treatment profiles, this marker constellation was concordantly associated with shorter DFS and OAS (P<0.001 and P=0.075 for cohort B and P=0.043 and P<0.001 for cohort C, respectively). In multivariate analysis, this algorithm was the main independent prognostic factor. Cohort B: DFS, P=0.0065, OAS, not significant; cohort C: DFS, P=0.026, OAS, P<0.001. CONCLUSION: Activated leukocyte cell adhesion molecule and OPN mRNA expression has a strong discriminative impact on survival within cancer patients with low or negative expression of ER and HER2, so called 'high-risk' breast cancers, and might help in identifying patients who could benefit from new treatment approaches like targeted therapies in the adjuvant setting. AD - Department of Gynecology, University Medical Center Hamburg-Eppendorf, Martinistr. 52, Hamburg D-20246, Germany. m.ihnen@uke.uni-hamburg.de FAU - Ihnen, M AU - Ihnen M FAU - Wirtz, R M AU - Wirtz RM FAU - Kalogeras, K T AU - Kalogeras KT FAU - Milde-Langosch, K AU - Milde-Langosch K FAU - Schmidt, M AU - Schmidt M FAU - Witzel, I AU - Witzel I FAU - Eleftheraki, A G AU - Eleftheraki AG FAU - Papadimitriou, C AU - Papadimitriou C FAU - Janicke, F AU - Janicke F FAU - Briassoulis, E AU - Briassoulis E FAU - Pectasides, D AU - Pectasides D FAU - Rody, A AU - Rody A FAU - Fountzilas, G AU - Fountzilas G FAU - Muller, V AU - Muller V LA - eng PT - Journal Article DEP - 20100824 PL - England TA - Br J Cancer JT - British journal of cancer JID - 0370635 RN - 0 (Activated-Leukocyte Cell Adhesion Molecule) RN - 0 (EIF3A protein, human) RN - 0 (Eukaryotic Initiation Factor-3) RN - 0 (RNA, Messenger) RN - 0 (Receptors, Estrogen) RN - 106441-73-0 (Osteopontin) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Activated-Leukocyte Cell Adhesion Molecule/*genetics MH - Adult MH - Aged MH - Breast Neoplasms/*genetics/mortality MH - Cluster Analysis MH - Decision Trees MH - Disease-Free Survival MH - Eukaryotic Initiation Factor-3 MH - Female MH - Humans MH - Middle Aged MH - Oligonucleotide Array Sequence Analysis MH - Osteopontin/*genetics MH - Prognosis MH - RNA, Messenger/metabolism MH - Receptor, erbB-2/*genetics MH - Receptors, Estrogen/*genetics MH - Risk PMC - PMC2965857 OID - NLM: PMC2965857 [Available on 09/28/11] EDAT- 2010/08/26 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/08/26 06:00 PMCR- 2011/09/28 PHST- 2010/08/24 [aheadofprint] AID - 6605840 [pii] AID - 10.1038/sj.bjc.6605840 [doi] PST - ppublish SO - Br J Cancer. 2010 Sep 28;103(7):1048-56. Epub 2010 Aug 24. PMID- 20736944 OWN - NLM STAT- MEDLINE DA - 20100929 DCOM- 20101025 LR - 20101102 IS - 1532-1827 (Electronic) IS - 0007-0920 (Linking) VI - 103 IP - 7 DP - 2010 Sep 28 TI - Prolactin serum levels and breast cancer: relationships with risk factors and tumour characteristics among pre- and postmenopausal women in a population-based case-control study from Poland. PG - 1097-102 AB - BACKGROUND: Previous prospective studies have found an association between prolactin (PRL) levels and increased risk of breast cancer. Using data from a population-based breast cancer case-control study conducted in two cities in Poland (2000-2003), we examined the association of PRL levels with breast cancer risk factors among controls and with tumour characteristics among the cases. METHODS: We analysed PRL serum levels among 773 controls without breast cancer matched on age and residence to 776 invasive breast cancer cases with available pretreatment serum. Tumours were centrally reviewed and prepared as tissue microarrays for immunohistochemical analysis. Breast cancer risk factors, assessed by interview, were related to serum PRL levels among controls using analysis of variance. Mean serum PRL levels by tumour characteristics are reported. These associations also were evaluated using polytomous logistic regression. RESULTS: Prolactin levels were associated with nulliparity in premenopausal (P=0.05) but not in postmenopausal women. Associations in postmenopausal women included an inverse association with increasing body mass index (P=0.0008) and direct association with use of recent/current hormone therapy (P=0.0006). In case-only analyses, higher PRL levels were more strongly associated with lobular compared with ductal carcinoma among postmenopausal women (P=0.02). Levels were not different by tumour size, grade, node involvement or oestrogen receptor, progesterone receptor, or human epidermal growth factor receptor 2 status. CONCLUSIONS: Our analysis demonstrates that PRL levels are higher among premenopausal nulliparous as compared with parous women. Among postmenopausal women, levels were higher among hormone users and lower among obese women. These results may have value in understanding the mechanisms underlying several breast cancer risk factor associations. AD - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, 6120 Executive Blvd (EPS), Suite 150E, MSC 7105, Bethesda, MD 20892, USA. badgerje@mail.nih.gov FAU - Faupel-Badger, J M AU - Faupel-Badger JM FAU - Sherman, M E AU - Sherman ME FAU - Garcia-Closas, M AU - Garcia-Closas M FAU - Gaudet, M M AU - Gaudet MM FAU - Falk, R T AU - Falk RT FAU - Andaya, A AU - Andaya A FAU - Pfeiffer, R M AU - Pfeiffer RM FAU - Yang, X R AU - Yang XR FAU - Lissowska, J AU - Lissowska J FAU - Brinton, L A AU - Brinton LA FAU - Peplonska, B AU - Peplonska B FAU - Vonderhaar, B K AU - Vonderhaar BK FAU - Figueroa, J D AU - Figueroa JD LA - eng GR - NIH0011788989/PHS HHS/United States PT - Journal Article PT - Research Support, N.I.H., Intramural DEP - 20100824 PL - England TA - Br J Cancer JT - British journal of cancer JID - 0370635 RN - 9002-62-4 (Prolactin) SB - IM MH - Adult MH - Breast Neoplasms/*blood MH - Case-Control Studies MH - Female MH - Humans MH - Middle Aged MH - Parity MH - Poland/epidemiology MH - Postmenopause MH - Pregnancy MH - Premenopause MH - Prolactin/*blood MH - Risk Factors PMC - PMC2965860 OID - NLM: PMC2965860 [Available on 09/28/11] EDAT- 2010/08/26 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/08/26 06:00 PMCR- 2011/09/28 PHST- 2010/08/24 [aheadofprint] AID - 6605844 [pii] AID - 10.1038/sj.bjc.6605844 [doi] PST - ppublish SO - Br J Cancer. 2010 Sep 28;103(7):1097-102. Epub 2010 Aug 24. PMID- 20709281 OWN - NLM STAT- MEDLINE DA - 20100816 DCOM- 20101105 IS - 1479-666X (Print) IS - 1479-666X (Linking) VI - 8 IP - 5 DP - 2010 Oct TI - Nipple discharge and the efficacy of duct cytology in evaluating breast cancer risk. PG - 252-8 AB - BACKGROUND: Nipple discharge accounts for up to 5% of referrals to breast surgical services. With the vast majority of breast carcinomas originating in the ductal system, symptomatic dysfunction of this system often raises disproportionate clinical concern. The aim of this study is firstly, to evaluate the clinical importance of nipple discharge as an indicator of underlying malignancy and secondly, to assess the diagnostic application of duct cytology in patients presenting with nipple discharge. STUDY DESIGN: We performed a retrospective analysis of all patients presenting with nipple discharge as their primary symptom to the symptomatic breast unit at a tertiary referral center over a 30-month period (n = 313). The Hospital Inpatient Enquiry (HIPE) System and BreastHealth database were used to identify our study cohort. Parameters evaluated included patient demographics, clinical presentation, clinical evaluation, radiological assessment and histological/cytological analysis. RESULTS: Three-hundred and thirteen patients presented with nipple discharge as their primary complaint. Invasive breast carcinoma was diagnosed by Triple Assessment in 5% of patients. 24% of patients presenting with nipple discharge underwent nipple aspiration and cytological analysis. Duct cytology was diagnostic of the underlying breast carcinoma in 50% of triple assessment diagnosed carcinoma. Four risk factors were identified as having a significant association with breast carcinoma, these included (a) age >50 years (p < 0.0001), (b) bloody nipple discharge (p < 0.008), (c) presence of a breast lump (p < 0.0001) and (d) single duct discharge (p < 0.006). CONCLUSIONS: Nipple discharge is a poor indicator of an underlying malignancy. Use of nipple aspiration and duct cytology for the assessment of nipple discharge is of limited diagnostic benefit. However, by utilizing the systematic, gold standard approach of Triple Assessment (clinical, radiological and cytological evaluation), the risk of underlying carcinoma can be accurately defined. CI - Copyright (c) 2010 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved. AD - Department of Breast & Endocrine Surgery, Mater Misericordiae University Hospital, Dublin, Ireland. roshdolan@hotmail.com FAU - Dolan, Roisin T AU - Dolan RT FAU - Butler, Joseph S AU - Butler JS FAU - Kell, Malcolm R AU - Kell MR FAU - Gorey, Thomas F AU - Gorey TF FAU - Stokes, Maurice A AU - Stokes MA LA - eng PT - Journal Article DEP - 20100513 PL - Scotland TA - Surgeon JT - The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland JID - 101168329 SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Algorithms MH - Biopsy, Fine-Needle MH - Breast Neoplasms/*diagnosis/epidemiology/pathology MH - Female MH - Humans MH - Middle Aged MH - Nipple Aspirate Fluid/*cytology MH - Risk Assessment MH - Risk Factors MH - Sensitivity and Specificity MH - Young Adult EDAT- 2010/08/17 06:00 MHDA- 2010/11/06 06:00 CRDT- 2010/08/17 06:00 PHST- 2010/01/20 [received] PHST- 2010/02/28 [revised] PHST- 2010/03/29 [accepted] PHST- 2010/05/13 [aheadofprint] AID - S1479-666X(10)00126-5 [pii] AID - 10.1016/j.surge.2010.03.005 [doi] PST - ppublish SO - Surgeon. 2010 Oct;8(5):252-8. Epub 2010 May 13. PMID- 20698054 OWN - NLM STAT- MEDLINE DA - 20100809 DCOM- 20101108 IS - 1473-5709 (Electronic) IS - 0959-8278 (Linking) VI - 19 IP - 5 DP - 2010 Sep TI - Micronutrient intake and breast cancer characteristics among postmenopausal women. PG - 360-5 AB - Few studies on micronutrients and postmenopausal breast cancer have examined the association with breast cancer characteristics. The aim of this study was to investigate the associations between vitamin C, vitamin E, folate and beta-carotene from diet and supplements and risk of postmenopausal breast cancer subtypes defined by histology (ductal/lobular), estrogen receptor (ER) and progesterone receptor (PGR) status. In a prospective cohort study of 26,224 postmenopausal women information on diet, supplements and lifestyle was collected through questionnaires. One thousand seventy-two cases were identified during follow-up. Incidence rate ratios of total breast cancers and breast cancer subtypes related to micronutrient intake were calculated using Cox proportional hazard analyses. This study found no association between overall breast cancer and any micronutrients, while some effects were shown when stratifying by breast cancer subtypes: dietary but not supplemental beta-carotene showed a protective effect against lobular breast cancer [incidence rate ratio (IRR): 0.72; 95% confidence interval (CI): 0.57-0.91]. Dietary vitamin E was associated with decreased risk of ER and PGR positive breast cancer (IRR: 0.50; 95% CI: 0.25-0.98) and dietary folate was associated with increased risk of ER and PGR positive breast cancer (IRR: 1.27; 95% CI: 1.03-1.95). This study found no effect of micronutrients on overall risk of postmenopausal breast cancer, but indicated possible effects of micronutrients in subgroups of breast cancer, with a potential beneficial effect of dietary beta-carotene in lobular breast cancer and dietary vitamin E in ER + PGR+ breast cancer and a potential harmful effect of dietary folate in ER+ PGR+ breast cancer. AD - Institute of Cancer Epidemiology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen O, Denmark. roswall@cancer.dk FAU - Roswall, Nina AU - Roswall N FAU - Olsen, Anja AU - Olsen A FAU - Christensen, Jane AU - Christensen J FAU - Dragsted, Lars O AU - Dragsted LO FAU - Overvad, Kim AU - Overvad K FAU - Tjonneland, Anne AU - Tjonneland A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Eur J Cancer Prev JT - European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) JID - 9300837 RN - 0 (Micronutrients) RN - 0 (Neoplasm Proteins) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 1406-18-4 (Vitamin E) RN - 50-81-7 (Ascorbic Acid) RN - 59-30-3 (Folic Acid) RN - 7235-40-7 (beta Carotene) SB - IM MH - Ascorbic Acid/*administration & dosage MH - *Breast Neoplasms/chemistry/epidemiology/pathology MH - Diet MH - Dietary Supplements MH - Female MH - Folic Acid/*administration & dosage MH - Follow-Up Studies MH - Humans MH - Micronutrients/*administration & dosage MH - Middle Aged MH - Neoplasm Proteins/analysis MH - *Postmenopause MH - Prospective Studies MH - Questionnaires MH - Receptors, Estrogen/analysis MH - Receptors, Progesterone/analysis MH - Risk MH - Vitamin E/*administration & dosage MH - beta Carotene/*administration & dosage EDAT- 2010/08/11 06:00 MHDA- 2010/11/09 06:00 CRDT- 2010/08/11 06:00 PST - ppublish SO - Eur J Cancer Prev. 2010 Sep;19(5):360-5. PMID- 20697093 OWN - NLM STAT- MEDLINE DA - 20100930 DCOM- 20101102 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 28 DP - 2010 Oct 1 TI - Human epidermal growth factor receptor 2 assessment in a case-control study: comparison of fluorescence in situ hybridization and quantitative reverse transcription polymerase chain reaction performed by central laboratories. PG - 4300-6 AB - PURPOSE: The optimal method to assess human epidermal growth factor receptor 2 (HER2) status remains highly controversial. Before reporting patient HER2 results, American Society of Clinical Oncology (ASCO)/College of American Pathologists (CAP) guidelines mandate that laboratories demonstrate >/= 95% concordance to another approved laboratory or methodology. Here, we compare central laboratory HER2 assessed by fluorescence in situ hybridization (FISH) and quantitative reverse transcriptase polymerase chain reaction (RT-PCR) using Oncotype DX in lymph node-negative, chemotherapy-untreated patients from a large Kaiser Permanente case-control study. PATIENTS AND METHODS: Breast cancer specimens from the Kaiser-Genomic Health study were examined. Central FISH assessment of HER2 amplification and polysomy 17 was conducted by PhenoPath Laboratories (ratios > 2.2, 1.8 to 2.2, and < 1.8 define HER2 positive, HER2 equivocal, and HER2 negative, respectively). HER2 expression by RT-PCR was conducted using Oncotype DX by Genomic Health (normalized expression units >/= 11.5, 10.7 to < 11.5, and < 10.7 define HER2 positive, HER2 equivocal, and HER2 negative, respectively). Concordance analyses followed ASCO/CAP guidelines. RESULTS: HER2 concordance by central FISH and central RT-PCR was 97% (95% CI, 96% to 99%). Twelve percent (67 of 568 patients) and 11% (60 of 568 patients) of patients were HER2 positive by RT-PCR and FISH, respectively. HER2-positive patients had increased odds of dying from breast cancer compared with HER2-negative patients. Polysomy 17 was demonstrated in 12.5% of all patients and 33% of FISH-positive patients. Nineteen of 20 FISH-positive patients with polysomy 17 were also RT-PCR HER2 positive. Although not statistically significantly different, HER2-positive/polysomy 17 patients tended to have the worst prognosis, followed by HER2-positive/eusomic, HER2-negative/polysomy 17, and HER2-negative/eusomic patients. CONCLUSION: There is a high degree of concordance between central FISH and quantitative RT-PCR using Oncotype DX for HER2 status, and the assay warrants additional study in a trastuzumab-treated population. AD - University of California, San Francisco, 1600 Divisadero St, Rm R200, San Francisco, CA 94063, USA. rbaehner@genomichealth.com FAU - Baehner, Frederick L AU - Baehner FL FAU - Achacoso, Ninah AU - Achacoso N FAU - Maddala, Tara AU - Maddala T FAU - Shak, Steve AU - Shak S FAU - Quesenberry, Charles P Jr AU - Quesenberry CP Jr FAU - Goldstein, Lynn C AU - Goldstein LC FAU - Gown, Allen M AU - Gown AM FAU - Habel, Laurel A AU - Habel LA LA - eng PT - Comparative Study PT - Journal Article DEP - 20100809 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Tumor Markers, Biological) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CIN - J Clin Oncol. 2010 Oct 1;28(28):4293-5. PMID: 20697085 CIN - J Clin Oncol. 2010 Oct 1;28(28):4289-92. PMID: 20697080 MH - Adult MH - Breast Neoplasms/*diagnosis/genetics/metabolism/mortality MH - California/epidemiology MH - Case-Control Studies MH - Chromosomes, Human, Pair 17 MH - False Negative Reactions MH - False Positive Reactions MH - Female MH - Humans MH - In Situ Hybridization, Fluorescence/*methods MH - Laboratories MH - Logistic Models MH - Middle Aged MH - Pathology, Clinical MH - Prognosis MH - Receptor, erbB-2/*metabolism MH - Registries MH - Reverse Transcriptase Polymerase Chain Reaction/*methods MH - Sensitivity and Specificity MH - Tumor Markers, Biological/metabolism EDAT- 2010/08/11 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/08/11 06:00 PHST- 2010/08/09 [aheadofprint] AID - JCO.2009.24.8211 [pii] AID - 10.1200/JCO.2009.24.8211 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 1;28(28):4300-6. Epub 2010 Aug 9. PMID- 20697085 OWN - NLM STAT- MEDLINE DA - 20100930 DCOM- 20101102 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 28 DP - 2010 Oct 1 TI - Human epidermal growth factor receptor 2 testing in 2010: does chromosome 17 centromere copy number make any difference? PG - 4293-5 FAU - Ross, Jeffrey S AU - Ross JS LA - eng PT - Comment PT - Editorial DEP - 20100809 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Antibodies, Monoclonal) RN - 0 (Antineoplastic Agents) RN - 0 (Quinazolines) RN - 0 (lapatinib) RN - 0 (trastuzumab) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CON - J Clin Oncol. 2010 Oct 1;28(28):4307-15. PMID: 20697084 CON - J Clin Oncol. 2010 Oct 1;28(28):4300-6. PMID: 20697093 CON - J Clin Oncol. 2010 Oct 1;28(28):4289-92. PMID: 20697080 MH - Antibodies, Monoclonal/therapeutic use MH - Antineoplastic Agents/therapeutic use MH - Breast Neoplasms/*diagnosis/drug therapy/*genetics MH - Centromere MH - *Chromosomes, Human, Pair 17 MH - Clinical Trials as Topic MH - False Negative Reactions MH - False Positive Reactions MH - Female MH - Humans MH - Immunohistochemistry MH - Practice Guidelines as Topic MH - Quinazolines/therapeutic use MH - Receptor, erbB-2/*genetics EDAT- 2010/08/11 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/08/11 06:00 PHST- 2010/08/09 [aheadofprint] AID - JCO.2010.29.6673 [pii] AID - 10.1200/JCO.2010.29.6673 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 1;28(28):4293-5. Epub 2010 Aug 9. PMID- 20697084 OWN - NLM STAT- MEDLINE DA - 20100930 DCOM- 20101102 IS - 1527-7755 (Electronic) IS - 0732-183X (Linking) VI - 28 IP - 28 DP - 2010 Oct 1 TI - HER2 and chromosome 17 effect on patient outcome in the N9831 adjuvant trastuzumab trial. PG - 4307-15 AB - PURPOSE: We examined associations between tumor characteristics (human epidermal growth factor receptor 2 [HER2] protein expression, HER2 gene and chromosome 17 copy number, hormone receptor status) and disease-free survival (DFS) of patients in the N9831 adjuvant trastuzumab trial. PATIENTS AND METHODS: All patients (N = 1,888) underwent chemotherapy with doxorubicin and cyclophosphamide, followed by weekly paclitaxel with or without concurrent trastuzumab. HER2 status was determined by immunohistochemistry (IHC) and fluorescent in situ hybridization (FISH) at a central laboratory, Mayo Clinic, Rochester, MN. Patients with conflicting local positive HER2 expression results but normal central laboratory testing were included in the analyses (n = 103). RESULTS: Patients with HER2-positive tumors (IHC 3+, FISH HER2/centromere 17 ratio >/= 2.0, or both) benefited from trastuzumab, with hazard ratios (HRs) of 0.46, 0.49, and 0.45, respectively (all P < .0001). Patients with HER2-amplified tumors with polysomic (p17) or normal (n17) chromosome 17 copy number also benefited from trastuzumab, with HRs of 0.52 and 0.37, respectively (P < .006). Patients who received chemotherapy alone and had HER2-amplified and p17 tumors had a longer DFS than those who had n17 (78% v 68%; P = .04), irrespective of hormone receptor status or tumor grade. Patients with HER2-normal tumors by central testing (n = 103) seemed to benefit from trastuzumab, but the difference was not statistically significant (HR, 0.51; P = .14). Patients with hormone receptor-positive or -negative tumors benefited from the addition of trastuzumab, with HRs of 0.42 (P = .005) and 0.60 (P = .0001), respectively. CONCLUSION: These results confirm that IHC or FISH HER2 testing is appropriate for patient selection for adjuvant trastuzumab therapy. Trastuzumab benefit seemed independent of HER2/centromere 17 ratio and chromosome 17 copy number. AD - Serene M. and Frances C. Durling Professor of Medicine, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224, USA. perez.edith@mayo.edu FAU - Perez, Edith A AU - Perez EA FAU - Reinholz, Monica M AU - Reinholz MM FAU - Hillman, David W AU - Hillman DW FAU - Tenner, Kathleen S AU - Tenner KS FAU - Schroeder, Matthew J AU - Schroeder MJ FAU - Davidson, Nancy E AU - Davidson NE FAU - Martino, Silvana AU - Martino S FAU - Sledge, George W AU - Sledge GW FAU - Harris, Lyndsay N AU - Harris LN FAU - Gralow, Julie R AU - Gralow JR FAU - Dueck, Amylou C AU - Dueck AC FAU - Ketterling, Rhett P AU - Ketterling RP FAU - Ingle, James N AU - Ingle JN FAU - Lingle, Wilma L AU - Lingle WL FAU - Kaufman, Peter A AU - Kaufman PA FAU - Visscher, Daniel W AU - Visscher DW FAU - Jenkins, Robert B AU - Jenkins RB LA - eng GR - CA114740/CA/NCI NIH HHS/United States GR - CA129949/CA/NCI NIH HHS/United States GR - CA25224/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100809 PL - United States TA - J Clin Oncol JT - Journal of clinical oncology : official journal of the American Society of Clinical Oncology JID - 8309333 RN - 0 (Antibodies, Monoclonal) RN - 0 (trastuzumab) RN - 23214-92-8 (Doxorubicin) RN - 33069-62-4 (Paclitaxel) RN - 50-18-0 (Cyclophosphamide) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CIN - J Clin Oncol. 2010 Oct 1;28(28):4289-92. PMID: 20697080 CIN - J Clin Oncol. 2010 Oct 1;28(28):4293-5. PMID: 20697085 MH - Adult MH - Antibodies, Monoclonal/*administration & dosage MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Breast Neoplasms/*drug therapy/*genetics/pathology MH - *Chromosomes, Human, Pair 17 MH - Clinical Trials, Phase III as Topic MH - Cyclophosphamide/administration & dosage MH - Disease-Free Survival MH - Doxorubicin/administration & dosage MH - Female MH - Humans MH - Immunohistochemistry MH - In Situ Hybridization, Fluorescence MH - Laboratories MH - Lymphatic Metastasis MH - Middle Aged MH - Paclitaxel/administration & dosage MH - Pathology, Clinical MH - Proportional Hazards Models MH - Randomized Controlled Trials as Topic MH - Receptor, erbB-2/*genetics MH - Treatment Outcome PMC - PMC2954132 OID - NLM: PMC2954132 [Available on 10/01/11] EDAT- 2010/08/11 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/08/11 06:00 PMCR- 2011/10/01 PHST- 2010/08/09 [aheadofprint] AID - JCO.2009.26.2154 [pii] AID - 10.1200/JCO.2009.26.2154 [doi] PST - ppublish SO - J Clin Oncol. 2010 Oct 1;28(28):4307-15. Epub 2010 Aug 9. PMID- 20687957 OWN - NLM STAT- MEDLINE DA - 20100825 DCOM- 20101025 IS - 1472-6874 (Electronic) IS - 1472-6874 (Linking) VI - 10 DP - 2010 TI - Women's constructions of the 'right time' to consider decisions about risk-reducing mastectomy and risk-reducing oophorectomy. PG - 24 AB - BACKGROUND: Women who are notified they carry a BRCA1/2 mutation are presented with surgical options to reduce their risk of breast and ovarian cancer, including risk-reducing mastectomy (RRM) and risk-reducing oophorectomy (RRO). Growing evidence suggests that a sub-group of women do not make decisions about RRM and RRO immediately following genetic testing, but rather, consider these decisions years later. Women's perspectives on the timing of these decisions are not well understood. Accordingly, the purpose of this research was to describe how women construct the 'right time' to consider decisions about RRM and RRO. METHODS: In-depth interviews were conducted with 22 BRCA1/2 carrier women and analyzed using qualitative, constant comparative methods. RESULTS: The time that lapsed between receipt of genetic test results and receipt of RRM or RRO ranged from three months to nine years. The findings highlighted the importance of considering decisions about RRM and RRO one at a time. The women constructed the 'right time' to consider these decisions to be when: (1) decisions fit into their lives, (2) they had enough time to think about decisions, (3) they were ready emotionally to deal with the decisions and the consequences, (4) all the issues and conflicts were sorted out, (5) there were better options available, and (6) the health care system was ready for them. CONCLUSIONS: These findings offer novel insights relevant to health care professionals who provide decision support to women considering RRM and RRO. AD - School of Population and Public Health, University of British Columbia, Canada. fuchsia.howard@ubc.ca FAU - Howard, A Fuchsia AU - Howard AF FAU - Bottorff, Joan L AU - Bottorff JL FAU - Balneaves, Lynda G AU - Balneaves LG FAU - Kim-Sing, Charmaine AU - Kim-Sing C LA - eng GR - Canadian Institutes of Health Research/Canada PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100805 PL - England TA - BMC Womens Health JT - BMC women's health JID - 101088690 SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Body Image MH - Breast Neoplasms/genetics/*prevention & control/surgery MH - *Decision Making MH - Female MH - Genes, BRCA1 MH - Genes, BRCA2 MH - Genetic Predisposition to Disease/psychology MH - Genetic Testing/psychology MH - Humans MH - Mastectomy/*psychology MH - Middle Aged MH - Ovarian Neoplasms/genetics/*prevention & control/surgery MH - Ovariectomy/*psychology MH - Risk Reduction Behavior MH - Time Factors PMC - PMC2927493 OID - NLM: PMC2927493 EDAT- 2010/08/07 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/08/07 06:00 PHST- 2010/01/14 [received] PHST- 2010/08/05 [accepted] PHST- 2010/08/05 [aheadofprint] AID - 1472-6874-10-24 [pii] AID - 10.1186/1472-6874-10-24 [doi] PST - epublish SO - BMC Womens Health. 2010 Aug 5;10:24. PMID- 20664515 OWN - NLM STAT- MEDLINE DA - 20100728 DCOM- 20101112 IS - 1526-2359 (Electronic) IS - 1073-2748 (Linking) VI - 17 IP - 3 DP - 2010 Jul TI - Gene expression profiling in breast cancer. PG - 177-82 AB - BACKGROUND: Breast cancer is a heterogeneous group of different tumor subtypes that vary in prognosis and response to therapy. This heterogeneity has spawned an era of molecular assays striving to classify and thus predict outcome, thereby guiding the future in targeted personalized treatment strategies. METHODS: This article provides an overview of the development and application of molecular assays as applied to breast cancer. Differences in the technology used for these tests as well as scientific evidence supporting the validity of the gene expression profile are discussed. Examples of the clinical applicability of these assays are provided, but these represent only a fraction of the potential uses yet to be discovered. A comparison of the three most commonly used assays is included. RESULTS: Molecular assays have provided new genetic approaches to unravel the complexities of clinical specimens relevant to breast cancer treatment planning and assessment of outcome. In particular, on a molecular level specific to the woman's tumor, these assays allow a prediction of outcome (prognosis) in terms of low and high risk for the future development of distant metastatic disease. Additionally, one assay, Oncotype DX (Genomic Health Inc, Redwood City, CA), allows for the prediction of benefit of the addition of chemotherapy to hormone therapy alone. CONCLUSIONS: While incorporation of molecular assays into the treatment planning strategy of breast cancer continues to be a work in progress, this approach is evolving quickly due to strong scientific evidence to become standard of practice in the near future. The possibilities of these assays in terms of clinical investigation are limitless, but currently their general applicability is limited to less than half of the population of women presenting with breast cancer. AD - Department of Women's Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA. FAU - Turaga, Kiran AU - Turaga K FAU - Acs, Geza AU - Acs G FAU - Laronga, Christine AU - Laronga C LA - eng PT - Journal Article PT - Review PL - United States TA - Cancer Control JT - Cancer control : journal of the Moffitt Cancer Center JID - 9438457 SB - IM MH - Breast Neoplasms/*genetics MH - Female MH - Gene Expression MH - Gene Expression Profiling/*methods/trends MH - Humans MH - Molecular Biology/methods/trends EDAT- 2010/07/29 06:00 MHDA- 2010/11/13 06:00 CRDT- 2010/07/29 06:00 PST - ppublish SO - Cancer Control. 2010 Jul;17(3):177-82. PMID- 20664514 OWN - NLM STAT- MEDLINE DA - 20100728 DCOM- 20101112 IS - 1526-2359 (Electronic) IS - 1073-2748 (Linking) VI - 17 IP - 3 DP - 2010 Jul TI - A review of triple-negative breast cancer. PG - 173-6 AB - BACKGROUND: An estimated 1 million cases of breast cancer are diagnosed annually worldwide. Of these, more than 170,000 are described as triple-negative. Triple-negative breast cancer (TNBC) is defined by the lack of protein expression of estrogen receptor (ER) and progesterone receptor (PR) and the absence of HER2 protein overexpression. TNBC is a subtype of breast cancer that overlaps with the "basal-like" breast cancer. TNBC has significant clinical implications. METHODS: The epidemiology, diagnosis, clinical course, prognosis, and pathology of this subtype of breast cancer are reviewed. The authors compare the "triple-negative" and "basal-like" definitions of breast cancer. A discussion of both standard and experimental treatments for TNBC is included. RESULTS: The poor prognosis of high-grade TNBC relates to poor disease-free interval in the adjuvant setting, shortened progression-free survival in the metastatic setting, and the lack of targeted therapy. However, not all TNBCs are associated with a poor prognosis. CONCLUSIONS: Although chemotherapy is the main current treatment of this subtype of breast cancer, new agents such as PARP inhibitors, which show promise in the treatment of TNBC, are currently in clinical trials. AD - Department of Women's Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA. Roohi.Ismail-Khan@moffitt.org FAU - Ismail-Khan, Roohi AU - Ismail-Khan R FAU - Bui, Marilyn M AU - Bui MM LA - eng PT - Journal Article PT - Review PL - United States TA - Cancer Control JT - Cancer control : journal of the Moffitt Cancer Center JID - 9438457 RN - 0 (Antineoplastic Agents) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - EC 2.7.10.1 (ERBB2 protein, human) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Antineoplastic Agents/therapeutic use MH - Breast Neoplasms/*diagnosis/genetics/*therapy MH - Clinical Trials as Topic MH - Female MH - Humans MH - Prognosis MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics EDAT- 2010/07/29 06:00 MHDA- 2010/11/13 06:00 CRDT- 2010/07/29 06:00 PST - ppublish SO - Cancer Control. 2010 Jul;17(3):173-6. PMID- 20664511 OWN - NLM STAT- MEDLINE DA - 20100728 DCOM- 20101112 IS - 1526-2359 (Electronic) IS - 1073-2748 (Linking) VI - 17 IP - 3 DP - 2010 Jul TI - Molecular and functional imaging of breast cancer. PG - 143-55 AB - BACKGROUND: Significant efforts have been directed toward developing and enhancing imaging methods for the early detection, diagnosis, and characterization of small breast tumors. Molecular and functional imaging sets the stage for enhancement of current methodology. METHODS: Current imaging modalities are described based on the molecular characteristics of normal and malignant tissue. New molecular imaging methods that have the potential for clinical use are also discussed. RESULTS: Dynamic contrast-enhanced magnetic resonance imaging is more sensitive than mammography in BRCA1 carriers. It is used in screening and in the early evaluation of neoadjuvant therapy. Positron emission mammography is 91% sensitive and 93% specific in detecting primary breast cancers. Sentinel node scintigraphy is a key component of axillary lymph node evaluation. Other imaging modalities being studied include Tc99m sestamibi, radiolabeled thymidine or uridine, estrogen receptor imaging, magnetic resonance spectroscopy, and diffusion magnetic resonance imaging. CONCLUSIONS: Molecular and functional imaging of the breast will likely alter clinical practice in diagnosing and staging primary breast cancer and assessing response to therapy since it will provide earlier information regarding the underlying biology of individual breast cancers, tumor stage, potential treatment strategies, and biomarkers for early evaluation of treatment effects. AD - H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida, USA. FAU - Tafreshi, Narges K AU - Tafreshi NK FAU - Kumar, Virendra AU - Kumar V FAU - Morse, David L AU - Morse DL FAU - Gatenby, Robert A AU - Gatenby RA LA - eng PT - Journal Article PT - Review PL - United States TA - Cancer Control JT - Cancer control : journal of the Moffitt Cancer Center JID - 9438457 SB - IM MH - Breast Neoplasms/*diagnosis MH - Diagnostic Imaging/*methods MH - Female MH - Humans MH - Magnetic Resonance Imaging/methods MH - Mammography/methods MH - Positron-Emission Tomography/methods EDAT- 2010/07/29 06:00 MHDA- 2010/11/13 06:00 CRDT- 2010/07/29 06:00 PST - ppublish SO - Cancer Control. 2010 Jul;17(3):143-55. PMID- 20663721 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1878-0261 (Electronic) IS - 1574-7891 (Linking) VI - 4 IP - 4 DP - 2010 Aug TI - Molecular diversity in ductal carcinoma in situ (DCIS) and early invasive breast cancer. PG - 357-68 AB - Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer where cells restricted to the ducts exhibit an atypical phenotype. Some DCIS lesions are believed to rapidly transit to invasive ductal carcinomas (IDCs), while others remain unchanged. Existing classification systems for DCIS fail to identify those lesions that transit to IDC. We studied gene expression patterns of 31 pure DCIS, 36 pure invasive cancers and 42 cases of mixed diagnosis (invasive cancer with an in situ component) using Agilent Whole Human Genome Oligo Microarrays 44k. Six normal breast tissue samples were also included as controls. qRT-PCR was used for validation. All DCIS and invasive samples could be classified into the "intrinsic" molecular subtypes defined for invasive breast cancer. Hierarchical clustering establishes that samples group by intrinsic subtype, and not by diagnosis. We observed heterogeneity in the transcriptomes among DCIS of high histological grade and identified a distinct subgroup containing seven of the 31 DCIS samples with gene expression characteristics more similar to advanced tumours. A set of genes independent of grade, ER-status and HER2-status was identified by logistic regression that univariately classified a sample as belonging to this distinct DCIS subgroup. qRT-PCR of single markers clearly separated this DCIS subgroup from the other DCIS, and contains samples from several histopathological and intrinsic molecular subtypes. The genes that differentiate between these two types of DCIS suggest several processes related to the re-organisation of the microenvironment. This raises interesting possibilities for identification of DCIS lesions both with and without invasive characteristics, which potentially could be used in clinical assessment of a woman's risk of progression, and lead to improved management that would avoid the current over- and under-treatment of patients. CI - (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. AD - Department of Genetics, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Montebello, 0310 Oslo, Norway. aslauam@gmail.com FAU - Muggerud, Aslaug Aamodt AU - Muggerud AA FAU - Hallett, Michael AU - Hallett M FAU - Johnsen, Hilde AU - Johnsen H FAU - Kleivi, Kristine AU - Kleivi K FAU - Zhou, Wenjing AU - Zhou W FAU - Tahmasebpoor, Simin AU - Tahmasebpoor S FAU - Amini, Rose-Marie AU - Amini RM FAU - Botling, Johan AU - Botling J FAU - Borresen-Dale, Anne-Lise AU - Borresen-Dale AL FAU - Sorlie, Therese AU - Sorlie T FAU - Warnberg, Fredrik AU - Warnberg F LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100626 PL - Netherlands TA - Mol Oncol JT - Molecular oncology JID - 101308230 RN - 0 (Receptors, Estrogen) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Breast Neoplasms/*genetics/*pathology MH - Carcinoma, Ductal, Breast/*genetics/*pathology MH - Carcinoma, Intraductal, Noninfiltrating/*genetics/*pathology MH - Cluster Analysis MH - Comparative Genomic Hybridization MH - Disease Progression MH - Female MH - Gene Expression Profiling MH - Humans MH - Microarray Analysis MH - Middle Aged MH - Multigene Family MH - Neoplasm Invasiveness MH - Receptor, erbB-2/genetics MH - Receptors, Estrogen/genetics EDAT- 2010/07/29 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/07/29 06:00 PHST- 2010/04/29 [received] PHST- 2010/06/14 [revised] PHST- 2010/06/17 [accepted] PHST- 2010/06/26 [aheadofprint] AID - S1574-7891(10)00059-1 [pii] AID - 10.1016/j.molonc.2010.06.007 [doi] PST - ppublish SO - Mol Oncol. 2010 Aug;4(4):357-68. Epub 2010 Jun 26. PMID- 20663177 OWN - NLM STAT- MEDLINE DA - 20100804 DCOM- 20101028 IS - 1756-9966 (Electronic) IS - 0392-9078 (Linking) VI - 29 DP - 2010 TI - Association of sulfotransferase SULT1A1 with breast cancer risk: a meta-analysis of case-control studies with subgroups of ethnic and menopausal statue. PG - 101 AB - BACKGROUND: Sulfotransferase (SULT) plays an important role in the formation of estrogen which is usually conferred as a risk factor for breast cancer. Polymorphism of the SULT1A1 may be closely associated with breast cancer. However, studies on the association between polymorphism and breast cancer have yielded inconsistent results. We performed a meta-analysis including ethnic subgroup and menopausal statue subgroup to investigate the association of SULT1A1 Arg213His polymorphism with breast cancer. METHODS: PubMed, EBSCO and Web of Science databases were searched for the correlative articles up to January 2010 (10362 breast cancer patients and 14250 controls). The risk (odds ratio, OR) was used to estimate the association between SULT1A1 polymorphism and breast cancer risk. All of the data from each study use either fixed-effects or random-effects. RESULTS: We found that SULT1A1 Arg213His had no exact effect to increase the risk of breast cancer (OR = 1.07, 95% CI: 0.97-1.17, P = 0.164), but it did increase the risk of breast cancer among postmenopausal women in the dominant model (OR = 1.28, 95%CI: 1.04-1.58, P = 0.019). No similar effect was found among premenopausal breast cancer women (OR = 1.06, 95%CI: 0.88-1.27, P = 0.537). There was a significant increase in breast cancer risk among Asian women (OR = 2.03, 95% CI: 1.00-4.14, P = 0.051) but not Caucasian women in recessive model. There was publication bias among postmenopausal women subgroup (P = 0.002), however by using the trim and fill method, if the publication bias was the only source of the funnel plot asymmetry, it needed two more studies to be symmetrical. The value of Log OR did not change too much after the adjustment and the fail-safe number of missing studies that would bring the P-value changed was 17. CONCLUSIONS: We concluded that the polymorphism of SULT1A1 Arg213His might be one of the high risk factors for breast cancer in Asian women and in postmenopausal women for all races. We should point out that the publication bias among postmenopausal women may partly account for the result, but the conclusion might not affected deeply by the publication bias. AD - Department of Breast Surgery, Shanghai Cancer Hospital/Cancer Institute, Fudan University, Shanghai 200032, China. FAU - Jiang, Yiwei AU - Jiang Y FAU - Zhou, Liheng AU - Zhou L FAU - Yan, Tingting AU - Yan T FAU - Shen, Zhenzhou AU - Shen Z FAU - Shao, Zhimin AU - Shao Z FAU - Lu, Jinsong AU - Lu J LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100721 PL - England TA - J Exp Clin Cancer Res JT - Journal of experimental & clinical cancer research : CR JID - 8308647 RN - EC 2.8.2.1 (Arylsulfotransferase) RN - EC 2.8.2.1 (SULT1A1 protein, human) SB - IM MH - Arylsulfotransferase/*genetics MH - Breast Neoplasms/classification/*ethnology/*genetics MH - Case-Control Studies MH - Female MH - Humans MH - Polymorphism, Genetic/*genetics MH - *Postmenopause MH - Prognosis PMC - PMC2914670 OID - NLM: PMC2914670 EDAT- 2010/07/29 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/29 06:00 PHST- 2010/04/23 [received] PHST- 2010/07/21 [accepted] PHST- 2010/07/21 [aheadofprint] AID - 1756-9966-29-101 [pii] AID - 10.1186/1756-9966-29-101 [doi] PST - epublish SO - J Exp Clin Cancer Res. 2010 Jul 21;29:101. PMID- 20661408 OWN - NLM STAT- MEDLINE DA - 20100727 DCOM- 20101115 IS - 1936-2625 (Electronic) IS - 1936-2625 (Linking) VI - 3 IP - 6 DP - 2010 TI - p16INK4a expression in basal-like breast carcinoma. PG - 600-7 AB - BLBC represents a distinctive group of invasive breast carcinomas with specific genotype and immunoprofile. BLBC is usually defined by gene expression profiling and is currently associated with poor outcome. BLBCs are estrogen receptor (ER) negative, progesterone receptor (PgR) negative, HER2 negative, and usually show a variable expression of basal cytokeratins (CKs), EGFR and CD117. p16(INK4a) is a tumor suppressor protein, encoded by the CDKN2A gene, which regulates cell cycle. The reported association of abnormalities in the p16/Rb pathway with increased risk of malignancy prompted us to determine the expression of p16(INK4a) in a group of BLBC; the results were compared with a group of high-grade invasive carcinoma (HG-IC) of breast. Tissue microarrays (TMA) were constructed in triplicate including 18 BLBC and 18 HG-IC. All BLBC cases were ER-/PgR-/HER2-. Seventeen (94%) BLBC were CK 5/6+/CK 14+; 14 (78%) BLCB showed EGFR expression and 13 (72%) were CD117 positive. BLBCs showed a strong positive reaction with p16(INK4a) antibody in 16 of 18 (89%) cases. Although the significance of p16(INK4a) expression in breast cancer is not fully understood, we have shown that p16(INK4a) is strongly expressed in breast cancers with basal-like phenotype. Since it is known that p16(INK4a) is associated with aggressive behavior in human carcinomas, these data suggest that p16(INK4a) play a role in the poor prognosis of BLBC. AD - Department of Pathology, MetroHealth Medical Center-Case Western Reserve University, Cleveland, OH 44109, USA. olga.bohn@gmail.com FAU - Bohn, Olga L AU - Bohn OL FAU - Fuertes-Camilo, Mariana AU - Fuertes-Camilo M FAU - Navarro, Leticia AU - Navarro L FAU - Saldivar, Jesus AU - Saldivar J FAU - Sanchez-Sosa, Sergio AU - Sanchez-Sosa S LA - eng PT - Journal Article DEP - 20100630 PL - United States TA - Int J Clin Exp Pathol JT - International journal of clinical and experimental pathology JID - 101480565 RN - 0 (Cyclin-Dependent Kinase Inhibitor p16) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Breast Neoplasms/genetics/*metabolism/pathology MH - Cyclin-Dependent Kinase Inhibitor p16/*biosynthesis/genetics MH - Female MH - Gene Expression MH - *Gene Expression Profiling MH - Humans MH - Immunohistochemistry MH - Neoplasms, Basal Cell/genetics/*metabolism/pathology MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics MH - Tissue Array Analysis PMC - PMC2907122 OID - NLM: PMC2907122 EDAT- 2010/07/28 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/07/28 06:00 PHST- 2010/06/07 [received] PHST- 2010/06/26 [accepted] PHST- 2010/06/30 [epublish] PST - epublish SO - Int J Clin Exp Pathol. 2010 Jun 30;3(6):600-7. PMID- 20647319 OWN - NLM STAT- MEDLINE DA - 20100816 DCOM- 20101110 IS - 1538-7445 (Electronic) IS - 0008-5472 (Linking) VI - 70 IP - 16 DP - 2010 Aug 15 TI - A KRAS-variant in ovarian cancer acts as a genetic marker of cancer risk. PG - 6509-15 AB - Ovarian cancer (OC) is the single most deadly form of women's cancer, typically presenting as an advanced disease at diagnosis in part due to a lack of known risk factors or genetic markers of risk. The KRAS oncogene and altered levels of the microRNA (miRNA) let-7 are associated with an increased risk of developing solid tumors. In this study, we investigated a hypothesized association between an increased risk of OC and a variant allele of KRAS at rs61764370, referred to as the KRAS-variant, which disrupts a let-7 miRNA binding site in this oncogene. Specimens obtained were tested for the presence of the KRAS-variant from nonselected OC patients in three independent cohorts, two independent ovarian case-control studies, and OC patients with hereditary breast and ovarian cancer syndrome (HBOC) as well as their family members. Our results indicate that the KRAS-variant is associated with more than 25% of nonselected OC cases. Further, we found that it is a marker for a significant increased risk of developing OC, as confirmed by two independent case-control analyses. Lastly, we determined that the KRAS-variant was present in 61% of HBOC patients without BRCA1 or BRCA2 mutations, previously considered uninformative, as well as in their family members with cancer. Our findings strongly support the hypothesis that the KRAS-variant is a genetic marker for increased risk of developing OC, and they suggest that the KRAS-variant may be a new genetic marker of cancer risk for HBOC families without other known genetic abnormalities. CI - (c)2010 AACR. AD - Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. FAU - Ratner, Elena AU - Ratner E FAU - Lu, Lingeng AU - Lu L FAU - Boeke, Marta AU - Boeke M FAU - Barnett, Rachel AU - Barnett R FAU - Nallur, Sunitha AU - Nallur S FAU - Chin, Lena J AU - Chin LJ FAU - Pelletier, Cory AU - Pelletier C FAU - Blitzblau, Rachel AU - Blitzblau R FAU - Tassi, Renata AU - Tassi R FAU - Paranjape, Trupti AU - Paranjape T FAU - Hui, Pei AU - Hui P FAU - Godwin, Andrew K AU - Godwin AK FAU - Yu, Herbert AU - Yu H FAU - Risch, Harvey AU - Risch H FAU - Rutherford, Thomas AU - Rutherford T FAU - Schwartz, Peter AU - Schwartz P FAU - Santin, Alessandro AU - Santin A FAU - Matloff, Ellen AU - Matloff E FAU - Zelterman, Daniel AU - Zelterman D FAU - Slack, Frank J AU - Slack FJ FAU - Weidhaas, Joanne B AU - Weidhaas JB LA - eng GR - CA131301-01A1/CA/NCI NIH HHS/United States GR - K08 CA124484/CA/NCI NIH HHS/United States GR - R01 CA122728-01A2/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100720 PL - United States TA - Cancer Res JT - Cancer research JID - 2984705R RN - 0 (Genetic Markers) RN - 0 (Tumor Markers, Biological) SB - IM MH - Adult MH - Aged MH - Breast Neoplasms/genetics MH - Case-Control Studies MH - Female MH - *Genes, ras MH - Genetic Markers MH - Genetic Predisposition to Disease MH - Genetic Variation MH - Humans MH - Middle Aged MH - Ovarian Neoplasms/*genetics MH - Tumor Markers, Biological/*genetics PMC - PMC2923587 MID - NIHMS216485 OID - NLM: NIHMS216485 [Available on 08/01/11] OID - NLM: PMC2923587 [Available on 08/01/11] EDAT- 2010/07/22 06:00 MHDA- 2010/11/11 06:00 CRDT- 2010/07/22 06:00 PMCR- 2011/08/01 PHST- 2010/07/20 [aheadofprint] AID - 0008-5472.CAN-10-0689 [pii] AID - 10.1158/0008-5472.CAN-10-0689 [doi] PST - ppublish SO - Cancer Res. 2010 Aug 15;70(16):6509-15. Epub 2010 Jul 20. PMID- 20641049 OWN - NLM STAT- MEDLINE DA - 20101004 DCOM- 20101028 IS - 1365-2168 (Electronic) IS - 0007-1323 (Linking) VI - 97 IP - 11 DP - 2010 Nov TI - Comparison of three mathematical models for predicting the risk of additional axillary nodal metastases after positive sentinel lymph node biopsy in early breast cancer. PG - 1646-52 AB - BACKGROUND: Women with breast cancer and a positive axillary sentinel lymph node (SLN) are recommended to undergo complete axillary lymph node dissection; however, further nodal disease is not always present. Mathematical models have been constructed to determine the risk of metastatic disease; three of these were evaluated independently. METHODS: Data from 108 women with breast cancer who had a positive SLN biopsy and completion axillary lymph node dissection were used. Measurements of additional parameters over those usually determined (such as size of SLN metastasis) were assessed under the supervision of two pathologists. These data were used to determine the predicted risk of non-SLN metastases using three mathematical models (from Memorial Sloan-Kettering Cancer Center (MSKCC), Cambridge University and Stanford University) and a comparison made with the observed findings. Analyses were made using the area under the receiver operating characteristic (ROC) curve (AUC). RESULTS: Some 53 (49.1 per cent) of 108 patients had a positive non-sentinel axillary lymph node metastasis. The AUC values were 0.63, 0.72 and 0.67 for the MSKCC, Cambridge and Stanford nomograms respectively. CONCLUSION: This independent comparison found no significant difference between the models, although the Cambridge model had the advantage of requiring fewer measurements with a more accurate predictive performance. CI - Copyright (c) 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. AD - Department of Histopathology, University College Hospital, London, UK. FAU - Moghaddam, Y AU - Moghaddam Y FAU - Falzon, M AU - Falzon M FAU - Fulford, L AU - Fulford L FAU - Williams, N R AU - Williams NR FAU - Keshtgar, M R AU - Keshtgar MR LA - eng PT - Comparative Study PT - Journal Article PL - England TA - Br J Surg JT - The British journal of surgery JID - 0372553 SB - AIM SB - IM MH - Area Under Curve MH - Axilla MH - Breast Neoplasms/*pathology/surgery MH - Cohort Studies MH - Female MH - Humans MH - Lymph Nodes/*pathology MH - Lymphatic Metastasis MH - *Nomograms MH - Risk Factors MH - Sensitivity and Specificity MH - *Sentinel Lymph Node Biopsy EDAT- 2010/07/20 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/20 06:00 AID - 10.1002/bjs.7181 [doi] PST - ppublish SO - Br J Surg. 2010 Nov;97(11):1646-52. PMID- 20632911 OWN - NLM STAT- MEDLINE DA - 20100716 DCOM- 20101028 IS - 1473-0766 (Electronic) IS - 0951-3590 (Linking) VI - 26 IP - 8 DP - 2010 Aug TI - Gynaecologic challenging issues in the management of BRCA mutation carriers: oral contraceptives, prophylactic salpingo-oophorectomy and hormone replacement therapy. PG - 568-77 AB - BRCA1 and BRCA2 mutation carriers have a 54-85% and 45% lifetime risk of developing breast cancer, respectively, and a 18-60% and 11-27% lifetime risk of developing ovarian cancer, respectively. Oral contraceptives (OCs) significantly reduce the risk of ovarian cancer also in BRCA1/BRCA2 mutation carriers. The association between OC use and breast cancer risk in these women is controversial. Some studies showed a modestly increased risk especially among BRCA1 mutation carriers. The risk appears to be greater for women who took OCs for at least 5 years and who took OCs before the age of 30 years. Other studies reported that duration of use before first full-term pregnancy has a positive association with breast cancer risk. Salpingo-oophorectomy reduces the risk of coelomic epithelial cancer of 80-95% and the risk of breast cancer of approximately 50%. BRCA1 and BRCA2 mutation carriers should be encouraged to undergo prophylactic bilateral salpingo-oophorectomy at the age of 35-40 years or when childbearing is complete. Short-term use of hormone replacement therapy may relieve menopausal symptoms and does not appear to affect the breast cancer risk reduction obtained with salpingo-oophorectomy. AD - Department of Procreative Medicine, Division of Gynecology and Obstetrics, University of Pisa, Pisa, Italy. a.gadducci@obgyn.med.unipi.it FAU - Gadducci, Angiolo AU - Gadducci A FAU - Biglia, Nicoletta AU - Biglia N FAU - Cosio, Stefania AU - Cosio S FAU - Sismondi, Piero AU - Sismondi P FAU - Genazzani, Andrea Riccardo AU - Genazzani AR LA - eng PT - Journal Article PT - Review PL - England TA - Gynecol Endocrinol JT - Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology JID - 8807913 RN - 0 (Contraceptives, Oral) SB - IM MH - Breast Neoplasms/*etiology/genetics MH - Contraceptives, Oral/adverse effects/*therapeutic use MH - Estrogen Replacement Therapy MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Humans MH - Mutation MH - Ovarian Neoplasms/*genetics/prevention & control MH - Ovariectomy EDAT- 2010/07/17 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/17 06:00 AID - 10.3109/09513590.2010.487609 [doi] PST - ppublish SO - Gynecol Endocrinol. 2010 Aug;26(8):568-77. PMID- 20615887 OWN - NLM STAT- MEDLINE DA - 20100709 DCOM- 20101028 IS - 1538-7755 (Electronic) IS - 1055-9965 (Linking) VI - 19 IP - 7 DP - 2010 Jul TI - Metabolic syndrome and breast cancer in the me-can (metabolic syndrome and cancer) project. PG - 1737-45 AB - BACKGROUND: Few studies have assessed the metabolic syndrome (MetS) as an entity in relation to breast cancer risk, and results have been inconsistent. We aimed to examine the association between MetS factors (individually and combined) and risk of breast cancer incidence and mortality. METHODS: Two hundred ninety thousand women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, blood pressure, and levels of glucose, cholesterol, and triglycerides. Relative risks (RR) of breast cancer were estimated using Cox proportional hazards regression for each MetS factor in quintiles and for standardized levels (z-scores) and for a composite z-score for the MetS. RESULTS: There were 4,862 incident cases of breast cancer and 633 deaths from breast cancer identified. In women below age 50, there was a decreased risk of incident cancer for the MetS (per 1-unit increment of z-score; RR, 0.83; 95% confidence interval, 0.76-0.90) as well as for the individual factors (except for glucose). The lowest risks were seen among the heaviest women. In women above age 60, there was an increased risk of breast cancer mortality for the MetS (RR, 1.23; 95% confidence interval, 1.04-1.45) and for blood pressure and glucose. The strongest association with mortality was seen for increased glucose concentrations. CONCLUSIONS: The MetS was associated with a decreased risk of incident breast cancer in women below age 50 with high body mass index, and with an increased risk of breast cancer mortality in women above 60. IMPACT: Lifestyle interventions as recommended for cardiovascular disease prevention may be of value to prevent breast cancer mortality in postmenopausal women. AD - Department of Public Health and Primary Health Care, University of Bergen, N-5018 Bergen, Norway. tone.bjorge@isf.uib.no FAU - Bjorge, Tone AU - Bjorge T FAU - Lukanova, Annekatrin AU - Lukanova A FAU - Jonsson, Hakan AU - Jonsson H FAU - Tretli, Steinar AU - Tretli S FAU - Ulmer, Hanno AU - Ulmer H FAU - Manjer, Jonas AU - Manjer J FAU - Stocks, Tanja AU - Stocks T FAU - Selmer, Randi AU - Selmer R FAU - Nagel, Gabriele AU - Nagel G FAU - Almquist, Martin AU - Almquist M FAU - Concin, Hans AU - Concin H FAU - Hallmans, Goran AU - Hallmans G FAU - Haggstrom, Christel AU - Haggstrom C FAU - Stattin, Par AU - Stattin P FAU - Engeland, Anders AU - Engeland A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Cancer Epidemiol Biomarkers Prev JT - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JID - 9200608 SB - IM MH - Adult MH - Age Factors MH - Aged MH - Austria/epidemiology MH - Body Mass Index MH - Breast Neoplasms/complications/*epidemiology MH - Cohort Studies MH - Female MH - Humans MH - Incidence MH - Metabolic Syndrome X/complications/*epidemiology MH - Middle Aged MH - Norway/epidemiology MH - Proportional Hazards Models MH - Prospective Studies MH - Risk MH - Risk Factors MH - Sweden/epidemiology EDAT- 2010/07/10 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/10 06:00 AID - 19/7/1737 [pii] AID - 10.1158/1055-9965.EPI-10-0230 [doi] PST - ppublish SO - Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1737-45. PMID- 20615886 OWN - NLM STAT- MEDLINE DA - 20100709 DCOM- 20101028 IS - 1538-7755 (Electronic) IS - 1055-9965 (Linking) VI - 19 IP - 7 DP - 2010 Jul TI - Specialty supplements and breast cancer risk in the VITamins And Lifestyle (VITAL) Cohort. PG - 1696-708 AB - BACKGROUND: Use of nonvitamin, nonmineral "specialty" supplements has increased substantially over recent decades. Several supplements may have anti-inflammatory or anticancer properties. Additionally, supplements taken for symptoms of menopause have been associated with reduced risk of breast cancer in two case-control studies. However, there have been no prospective studies of the association between the long-term use of these supplements and breast cancer risk. METHODS: Participants were female members of the VITamins And Lifestyle (VITAL) Cohort. Postmenopausal women, ages 50 to 76 years, who were residents of western Washington State, completed a 24-page baseline questionnaire in 2000 to 2002 (n = 35,016). Participants were queried on their recency (current versus past), frequency (days/week), and duration (years) of specialty supplement use. Incident invasive breast cancers (n = 880) from 2000 to 2007 were obtained from the Surveillance, Epidemiology, and End Results registry. Multivariable-adjusted hazards ratios (HR) and 95% confidence intervals (95% CI) were estimated by Cox proportional hazards models. RESULTS: Current use of fish oil was associated with reduced risk of breast cancer (HR, 0.68; 95% CI, 0.50-0.92). Ten-year average use was suggestive of reduced risk (P trend = 0.09). These results held for ductal but not lobular cancers. The remaining specialty supplements were not associated with breast cancer risk: Specifically, use of supplements sometimes taken for menopausal symptoms (black cohosh, dong quai, soy, or St. John's wort) was not associated with risk. CONCLUSIONS: Fish oil may be inversely associated with breast cancer risk. IMPACT: Fish oil is a potential candidate for chemoprevention studies. Until that time, it is not recommended for individual use for breast cancer prevention. AD - Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, M4-B402, Seattle, WA 98109-1024, USA. tbrasky@fhcrc.org FAU - Brasky, Theodore M AU - Brasky TM FAU - Lampe, Johanna W AU - Lampe JW FAU - Potter, John D AU - Potter JD FAU - Patterson, Ruth E AU - Patterson RE FAU - White, Emily AU - White E LA - eng GR - R01 CA142545-01/CA/NCI NIH HHS/United States GR - R01 CA142545-02/CA/NCI NIH HHS/United States GR - R01-CA142545/CA/NCI NIH HHS/United States GR - R25 CA094880-08/CA/NCI NIH HHS/United States GR - R25-CA94880/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - United States TA - Cancer Epidemiol Biomarkers Prev JT - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JID - 9200608 RN - 0 (Fish Oils) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Breast Neoplasms/*epidemiology/prevention & control MH - Cohort Studies MH - Dietary Supplements MH - Female MH - Fish Oils/*administration & dosage MH - Humans MH - Middle Aged MH - Prospective Studies MH - Risk Factors MH - Washington/epidemiology PMC - PMC2906099 MID - NIHMS206693 OID - NLM: NIHMS206693 [Available on 07/01/11] OID - NLM: PMC2906099 [Available on 07/01/11] EDAT- 2010/07/10 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/10 06:00 PMCR- 2011/07/01 AID - 19/7/1696 [pii] AID - 10.1158/1055-9965.EPI-10-0318 [doi] PST - ppublish SO - Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1696-708. PMID- 20603714 OWN - NLM STAT- MEDLINE DA - 20100713 DCOM- 20101028 IS - 1544-2241 (Electronic) IS - 1544-1873 (Linking) VI - 8 IP - 3 DP - 2010 Sep TI - New selective estrogen receptor modulators (SERMs) in development. PG - 151-3 AB - Selective estrogen receptor modulators (SERMs) or estrogen agonists/antagonists have shown promise in osteoporosis in that they have the potential to reduce the risk of fracture, and also reduce the risk of breast cancer. SERMs maybe classified according to their core structure, which is typically a variation of the 17 beta-estradiol template and subclassified according to the side chain at the helix 12 affector region. The best known are the triphenylethylenes such as tamoxifen, used in the management of breast cancer. However, the clinical application of this class of SERMs has been limited due to endometrial stimulation. A second class is the benzothiophenes such as raloxifene and arzoxifene, which have skeletal benefit with little, if any, uterine stimulation. Indole-based SERMs such as bazedoxifene have a 2-phenyl ring system that serves as a core binding unit. Other classes include benzopyrans and naphthalenes (eg, lasofoxifene). In this review article, I will discuss raloxifene and three new SERMs--arzoxifene, bazedoxifene, and lasofoxifene--that have been recently studied. I will discuss their effect on bone, breast, and the cardiovascular system, as well as on safety. AD - Cedars-Sinai/UCLA, 8641 Wilshire Boulevard, Suite 301, Beverly Hills, CA 90211, USA. stuarts@omcresearch.org FAU - Silverman, Stuart L AU - Silverman SL LA - eng PT - Journal Article PT - Review PL - United States TA - Curr Osteoporos Rep JT - Current osteoporosis reports JID - 101176492 RN - 0 (Bone Density Conservation Agents) RN - 0 (Indoles) RN - 0 (LY 353381) RN - 0 (Piperidines) RN - 0 (Pyrrolidines) RN - 0 (Selective Estrogen Receptor Modulators) RN - 0 (Tetrahydronaphthalenes) RN - 0 (Thiophenes) RN - 0 (bazedoxifene acetate) RN - 0 (cis-1R-(4'-pyrrolidinoethoxyphenyl)-2S-phenyl-6-hydroxy-1,2,3,4-tetrahydronaphth alene, tartrate salt) SB - IM MH - Bone Density Conservation Agents/adverse effects/*therapeutic use MH - Breast Neoplasms/epidemiology/prevention & control MH - Female MH - Humans MH - Indoles/adverse effects/therapeutic use MH - Osteoporosis/*drug therapy MH - Piperidines/adverse effects/therapeutic use MH - Pyrrolidines/adverse effects/therapeutic use MH - Risk Factors MH - Selective Estrogen Receptor Modulators/adverse effects/*therapeutic use MH - Tetrahydronaphthalenes/adverse effects/therapeutic use MH - Thiophenes/adverse effects/therapeutic use PMC - PMC2902741 OID - NLM: PMC2902741 EDAT- 2010/07/07 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/07/07 06:00 AID - 10.1007/s11914-010-0025-0 [doi] PST - ppublish SO - Curr Osteoporos Rep. 2010 Sep;8(3):151-3. PMID- 20593953 OWN - NLM STAT- MEDLINE DA - 20100702 DCOM- 20101101 IS - 1513-7368 (Print) IS - 1513-7368 (Linking) VI - 11 IP - 1 DP - 2010 TI - Pesticides and breast cancer risk: a comparison between developed and developing countries. PG - 173-80 AB - BACKGROUND: A large number of studies in Europe and US find little or no association between pesticides and breast cancer, adding to the increasingly dominant view that pesticides are not causally related to breast cancer. We investigated whether there are any differences in the levels of pesticides like dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethylene (DDE), polychlorinated biphenyls (PCB), hexachlorobenzene (HCB) and hexachlorocyclohexane (HCH) and their effect for the development of breast cancer between developed and developing countries. METHODS: A pubmed search for literature on pesticides, organochlorines, organophosphates and breast cancer risk from 1990 through 2009 was carried out. RESULTS: The level of pesticide exposure is higher in developing world than the developed world. DDT is found to be positively associated with breast cancer risk. Results for other pesticides are equivocal. There is a dearth of studies in developing countries, which cannot be made up for generalizing the results from developed countries to the developing and third world. CONCLUSIONS: More studies are needed in the developing and third world countries, investigating the relation between pesticides and breast cancer risk as the sheer amount of pesticides being relentlessly used in these countries due to lack of proper government regulations. AD - Department of Psychology, Kent State University, USA. FAU - Shakeel, Mohammed K AU - Shakeel MK FAU - George, Preethi Sara AU - George PS FAU - Jose, Jesna AU - Jose J FAU - Jose, Josna AU - Jose J FAU - Mathew, Aleyamma AU - Mathew A LA - eng PT - Comparative Study PT - Journal Article PL - Thailand TA - Asian Pac J Cancer Prev JT - Asian Pacific journal of cancer prevention : APJCP JID - 101130625 RN - 0 (Pesticides) RN - 0 (Polychlorinated Biphenyls) RN - 118-74-1 (Hexachlorobenzene) RN - 50-29-3 (DDT) RN - 58-89-9 (Lindane) SB - IM MH - Adult MH - Breast Neoplasms/blood/*epidemiology/pathology MH - Case-Control Studies MH - DDT/pharmacology MH - Developed Countries/*statistics & numerical data MH - Developing Countries/*statistics & numerical data MH - Environmental Exposure MH - Female MH - Hexachlorobenzene/pharmacology MH - Humans MH - Lindane/pharmacology MH - Meta-Analysis as Topic MH - Middle Aged MH - Pesticides/*pharmacology MH - Polychlorinated Biphenyls/pharmacology MH - Prognosis MH - Risk Factors EDAT- 2010/07/03 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/07/03 06:00 PST - ppublish SO - Asian Pac J Cancer Prev. 2010;11(1):173-80. PMID- 20593932 OWN - NLM STAT- MEDLINE DA - 20100702 DCOM- 20101101 IS - 1513-7368 (Print) IS - 1513-7368 (Linking) VI - 11 IP - 1 DP - 2010 TI - Roles of adiposity, lifetime physical activity and serum adiponectin in occurrence of breast cancer among Malaysian women in Klang Valley. PG - 61-6 AB - BACKGROUND: Lack of physical activities throughout life is related to obesity and is a risk factor of breast cancer, however, the associations of these factors with adiponectin in the occurrence of breast cancer have not been well investigated. OBJECTIVE: This study investigated the relationship between adiposity, lifetime physical activities and serum adiponectin as breast cancer risk factors among Malaysian women in Klang Valley, Malaysia. DESIGN: A case-control study was carried out among 70 newly diagnosed breast cancer patients and 138 controls aged 29 to 65 years old in Klang Valley. SUBJECTS: The inclusion criteria for both groups were not having menstruation for premenopausal women, no evidence of pregnancy, not lactating and no chronic diseases such as hypertension and diabetes at the time of data collection. In addition, the cases must be pathologically newly diagnosed with breast cancer (stage I to III) and not on any therapy for cancer, with the exception of surgery. The controls were matched with cases for age +/- 5 years and menopausal status. MEASUREMENTS: Subjects were interviewed to obtain information on socio-demography, health and reproductive history using a pretested questionnaire. Subjects were also asked on their engagement of physical activity since secondary school. Anthropometric parameters included height, weight, waist and hips were also measured. A total of 6 ml of fasting venous blood was drawn for analysis of serum adiponectin in duplicate using Linko Adiponectin ELISA Kit. Fasting blood glucose (FBG) and blood pressure were also measured. RESULTS: Mean body mass index (BMI) among cases and controls were not significantly different (p> 0.05) at 26.1 -/+ 4.8 kg/m2 and 25.3 -/+ 4.5 kg/m2, respectively. FBG among cases (6.3 -/+ 1.8 mmol/L) was higher than controls (5.6 -/+ 1.1 mmol/L) (p<0.05). Waist hip ratio (WHR) of cases (0.85 -/+ 0.07) was also higher than controls (0.80 -/+ 0.06) (p<0.05). Abdominal obesity (WHR > 0.85) increased risk of breast cancer by three folds [Adjusted OR 3.3 (95%CI 1.8-6.2)] (p<0.05). Adiponectin level was inversely related to waist circumference (r=-0.510, p=0.000), BMI (r=-0.448, p=0.000) and FBG (r=-0.290, p=0.026). Adiponectin level in cases (11.9 -/+ 4.8 microg/ml) were lower than controls (15.2 -/+ 7.3 microg/ml) (p<0.05). A greater reduction of breast cancer risk was observed with the increasing level of serum adiponectin level according to percentiles (p<0.05). Subjects with mean serum adiponectin level at the highest quintile (> 75th)( >or= 16.7 microg/ml) had 80% reduced risk of breast cancer [Adjusted OR 0.2 (0.0-0.6)](p<0.05). A higher percentage of cases (47%) had not engaged in any physical activity throughout life as compared to controls (19%)[Adjusted OR 3.7 (1.7-7.7)](p<0.001). CONCLUSIONS: Abdominal obesity and physical inactivity throughout life were associated with low serum adiponectin and breast cancer risk among subjects. Thus, it is essential for Malaysian women to be physically active and achieve a healthy waistline in order to increase serum adiponectin level and reduce breast cancer risk. AD - Department of Nutrition and Dietetic, Faculty of Allied Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia. suzana.shahar@gmail.com FAU - Shahar, Suzana AU - Shahar S FAU - Salleh, Rabeta Mohd AU - Salleh RM FAU - Ghazali, Ahmad Rohi AU - Ghazali AR FAU - Koon, Poh Bee AU - Koon PB FAU - Mohamud, Wan Nazaimoon Wan AU - Mohamud WN LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Thailand TA - Asian Pac J Cancer Prev JT - Asian Pacific journal of cancer prevention : APJCP JID - 101130625 RN - 0 (Adiponectin) SB - IM MH - Adiponectin/*blood MH - *Adiposity MH - Adolescent MH - Adult MH - Body Mass Index MH - Breast Neoplasms/*blood/epidemiology/*etiology MH - Case-Control Studies MH - *Exercise MH - Female MH - Humans MH - Incidence MH - Malaysia/epidemiology MH - Middle Aged MH - Pregnancy MH - Risk Factors MH - Waist-Hip Ratio MH - Young Adult EDAT- 2010/07/03 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/07/03 06:00 PST - ppublish SO - Asian Pac J Cancer Prev. 2010;11(1):61-6. PMID- 20587409 OWN - NLM STAT- MEDLINE DA - 20100630 DCOM- 20101029 IS - 1938-0666 (Electronic) IS - 1526-8209 (Linking) VI - 10 Suppl 1 DP - 2010 TI - Optimizing chemotherapy regimens for patients with early-stage breast cancer. PG - E8-15 AB - While moving toward a personalized treatment approach for early breast cancer, it is clear that treatment must be tailored specifically to the tumor's and patient's characteristics. Understanding the tumor's molecular signature and using validated prognostic and predictive tools can assist the oncologist in providing the optimal therapy. Through a shared decision process, a treatment plan must be formulated based on the tumor's biologic phenotype, taking into consideration the patient's comorbidities and preferences. This review summarizes the available tools that can assist in this process and provides an overview of the chemotherapy regimens approved for the adjuvant treatment of patients with early-stage breast cancer. AD - Fox Chase Cancer Center, Philadelphia, PA 19111-2412, USA. FAU - Dotan, Efrat AU - Dotan E FAU - Goldstein, Lori J AU - Goldstein LJ LA - eng PT - Journal Article PT - Review PL - United States TA - Clin Breast Cancer JT - Clinical breast cancer JID - 100898731 RN - 0 (Anthracyclines) RN - 0 (Diphosphonates) RN - 0 (Plasminogen Activator Inhibitor 1) RN - 0 (Tumor Markers, Biological) RN - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) SB - IM MH - Anthracyclines/therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/adverse effects/*therapeutic use MH - Breast Neoplasms/classification/*diagnosis/*drug therapy MH - Diphosphonates/therapeutic use MH - Female MH - Genes, erbB-2 MH - Genetic Predisposition to Disease/etiology MH - Humans MH - Neoplasm Staging MH - Plasminogen Activator Inhibitor 1/metabolism MH - Risk Assessment MH - Tumor Markers, Biological/metabolism MH - Urokinase-Type Plasminogen Activator/metabolism EDAT- 2010/07/01 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/07/01 06:00 AID - 060414Q362610130 [pii] AID - 10.3816/CBC.2010.s.002 [doi] PST - ppublish SO - Clin Breast Cancer. 2010;10 Suppl 1:E8-15. PMID- 20587408 OWN - NLM STAT- MEDLINE DA - 20100630 DCOM- 20101029 IS - 1938-0666 (Electronic) IS - 1526-8209 (Linking) VI - 10 Suppl 1 DP - 2010 TI - Lethal breast cancer. PG - E6-7 AD - Baylor Sammons Cancer Center, US Oncology, Texas Oncology, Dallas, TX, USA. FAU - O'Shaughnessy, Joyce A AU - O'Shaughnessy JA LA - eng PT - Introductory Journal Article PL - United States TA - Clin Breast Cancer JT - Clinical breast cancer JID - 100898731 RN - 0 (Cytokines) RN - 0 (Vascular Endothelial Growth Factor A) SB - IM MH - *Breast Neoplasms/genetics/metabolism MH - Cytokines/metabolism MH - Female MH - Genes, erbB-2 MH - Genetic Predisposition to Disease/etiology MH - Humans MH - Vascular Endothelial Growth Factor A/biosynthesis EDAT- 2010/07/01 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/07/01 06:00 AID - 0125213UH7334774 [pii] AID - 10.3816/CBC.2010.s.001 [doi] PST - ppublish SO - Clin Breast Cancer. 2010;10 Suppl 1:E6-7. PMID- 20587406 OWN - NLM STAT- MEDLINE DA - 20100630 DCOM- 20101029 IS - 1938-0666 (Electronic) IS - 1526-8209 (Linking) VI - 10 Suppl 1 DP - 2010 TI - Clinical updates on EGFR/HER targeted agents in early-stage breast cancer. PG - E38-46 AB - Recent updated reports from the large adjuvant trials in HER2-positive breast cancer indicate that the remarkable benefits of adding trastuzumab to chemotherapy appear, so far, to be sustained rather than transient. Other studies show that even small, node-negative, HER2-positive tumors carry some risk of recurrence and might benefit from trastuzumab-based adjuvant therapy. Evaluations of HER2 test results have examined the benefit of trastuzumab in cancers that exhibit focally positive gene amplification and also have raised the question of whether the criteria that correlate HER2 positivity with trastuzumab benefit in the adjuvant setting may be different from the criteria that apply in the treatment of metastatic disease. New results from trials combining targeted agents in the treatment of metastatic breast cancer provide strong rationale for the current adjuvant trials. In addition, neoadjuvant studies lend further support for combining targeted agents and may also provide an optimal setting to identify biomarkers that correlate with patient outcome. A new generation of therapies, including novel targeted agents and vaccines, is moving forward in clinical development and will be incorporated into adjuvant regimens in the future. AD - Lucille Parker Markey Cancer Center, University of Kentucky, Lexington 40536-0093, USA. FAU - Macrinici, Valentina AU - Macrinici V FAU - Romond, Edward AU - Romond E LA - eng PT - Journal Article PT - Review PL - United States TA - Clin Breast Cancer JT - Clinical breast cancer JID - 100898731 RN - 0 (Antibodies, Monoclonal) RN - 0 (Tumor Markers, Biological) RN - 0 (trastuzumab) RN - EC 2.7.10.1 (Receptor, Epidermal Growth Factor) SB - IM MH - Antibodies, Monoclonal/pharmacology/therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Brain Neoplasms/secondary MH - Breast Neoplasms/classification/*drug therapy/mortality MH - Chemotherapy, Adjuvant MH - Clinical Trials as Topic MH - Female MH - *Genes, erbB-2 MH - Humans MH - Neoadjuvant Therapy MH - Receptor, Epidermal Growth Factor/*analysis MH - Retrospective Studies MH - Tumor Markers, Biological/*analysis EDAT- 2010/07/01 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/07/01 06:00 AID - 00220L5L36657225 [pii] AID - 10.3816/CBC.2010.s.006 [doi] PST - ppublish SO - Clin Breast Cancer. 2010;10 Suppl 1:E38-46. PMID- 20587403 OWN - NLM STAT- MEDLINE DA - 20100630 DCOM- 20101029 IS - 1938-0666 (Electronic) IS - 1526-8209 (Linking) VI - 10 Suppl 1 DP - 2010 TI - Novel treatment approaches for triple-negative breast cancer. PG - E16-22 AB - Triple-negative breast cancers share an aggressive biology, marked by increased recurrence risk and poorer survival compared with hormone receptor-positive subtypes. Few therapeutic trials have specifically focused on triple-negative breast cancer, and the treatment of patients with early-stage triple-negative breast cancer has changed little in the past decade. Over this time, however, attention has shifted to treatment approaches based on molecular subtypes of breast cancer, and investigation into the mechanistic underpinnings of these distinct subtypes has exploded. Converging preclinical rationales combined with early provocative clinical efficacy has focused recent attention on strategies targeting DNA repair defects for the treatment of patients with triple-negative and BRCA mutation-associated breast cancers. These developments are very promising and suggest that major advances in the targeted treatment of patients with triple-negative breast cancer are in sight. This review provides an overview of the clinical features of triple-negative breast cancer and current treatment strategies in the adjuvant setting. Mechanisms of DNA repair and the DNA damage response are reviewed to provide background for understanding novel approaches targeting DNA repair defects in this disease with DNA-damaging chemotherapeutic agents and poly(ADP-ribose) polymerase inhibitors. Ongoing studies, including those investigating the role of antiangiogenic therapies, are also reviewed. AD - Department of Medicine, Stanford University School of Medicine, CA 94305-5820, USA. mtelli@stanford.edu FAU - Telli, Melinda L AU - Telli ML FAU - Ford, James M AU - Ford JM LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review PL - United States TA - Clin Breast Cancer JT - Clinical breast cancer JID - 100898731 RN - 0 (Angiogenesis Inhibitors) RN - 0 (DNA, Neoplasm) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Markers, Biological) RN - EC 2.4.2.30 (PARP1 protein, human) RN - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Angiogenesis Inhibitors/therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Breast Neoplasms/*classification/*drug therapy/genetics MH - DNA Damage MH - DNA Repair MH - DNA, Neoplasm MH - Female MH - Genes, BRCA1 MH - Humans MH - Poly(ADP-ribose) Polymerases/antagonists & inhibitors MH - Receptor, erbB-2/analysis/genetics MH - Receptors, Estrogen/analysis/genetics MH - Receptors, Progesterone/analysis/genetics MH - Tumor Markers, Biological/analysis EDAT- 2010/07/01 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/07/01 06:00 AID - 0667W6617W2N241V [pii] AID - 10.3816/CBC.2010.s.003 [doi] PST - ppublish SO - Clin Breast Cancer. 2010;10 Suppl 1:E16-22. PMID- 20583289 OWN - NLM STAT- MEDLINE DA - 20100701 DCOM- 20101029 IS - 1098-2272 (Electronic) IS - 0741-0395 (Linking) VI - 34 IP - 5 DP - 2010 Jul TI - Evaluating the power to discriminate between highly correlated SNPs in genetic association studies. PG - 463-8 AB - Neighboring common polymorphisms are often correlated (in linkage disequilibrium (LD)) as a result of shared ancestry. An association between a polymorphism and a disease trait may therefore be the indirect result of a correlated functional variant, and identifying the true causal variant(s) from an initial disease association is a major challenge in genetic association studies. Here, we present a method to estimate the sample size needed to discriminate between a functional variant of a given allele frequency and effect size, and other correlated variants. The sample size required to conduct such fine-scale mapping is typically 1-4 times larger than required to detect the initial association. Association studies in populations with different LD patterns can substantially improve the power to isolate the causal variant. An online tool to perform these calculations is available at http://moya.srl.cam.ac.uk/ocac/FineMappingPowerCalculator.html. CI - (c) 2010 Wiley-Liss, Inc. AD - Department of Public Health and Primary Care, University of Cambridge, Strangeways Research Laboratory, Worts Causeway, Cambridge, United Kingdom. FAU - Udler, Miriam S AU - Udler MS FAU - Tyrer, Jonathan AU - Tyrer J FAU - Easton, Douglas F AU - Easton DF LA - eng PT - Journal Article PL - United States TA - Genet Epidemiol JT - Genetic epidemiology JID - 8411723 RN - EC 2.7.1.112 (FGFR2 protein, human) RN - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2) SB - IM MH - Alleles MH - Breast Neoplasms/genetics MH - Female MH - *Genetic Predisposition to Disease MH - Genetic Variation MH - Genotype MH - Haplotypes MH - Humans MH - Internet MH - Linkage Disequilibrium MH - *Models, Genetic MH - *Models, Statistical MH - Polymorphism, Single Nucleotide/*genetics MH - Receptor, Fibroblast Growth Factor, Type 2/genetics MH - Sample Size EDAT- 2010/06/29 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/06/29 06:00 AID - 10.1002/gepi.20504 [doi] PST - ppublish SO - Genet Epidemiol. 2010 Jul;34(5):463-8. PMID- 20582464 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - DNA repair signature is associated with anthracycline response in triple negative breast cancer patients. PG - 189-96 AB - We hypothesized that a subset of sporadic triple negative (TN) breast cancer patients whose tumors have defective DNA repair similar to BRCA1-associated tumors are more likely to exhibit up-regulation of DNA repair-related genes, anthracycline-sensitivity, and taxane-resistance. We derived a defective DNA repair gene expression signature of 334 genes by applying a previously published BRCA1-associated expression pattern to three datasets of sporadic TN breast cancers. We confirmed a subset of 69 of the most differentially expressed genes by quantitative RT-PCR, using a low density custom array (LDA). Next, we tested the association of this DNA repair microarray signature expression with pathologic response in neoadjuvant anthracycline trials of FEC (n = 50) and AC (n = 16), or taxane-based TET chemotherapy (n = 39). Finally, we collected paraffin-fixed, formalin-embedded biopsies from TN patients who had received neoadjuvant AC (n = 28), and tested the utility of the LDA to discriminate response. Correlation between RNA expression measured by the microarrays and 69-gene LDA was ascertained. This defective DNA repair microarray gene expression pattern was significantly associated with anthracycline response and taxane resistance, with the area under the ordinary receiver operating characteristic curve (AUC) of 0.61 (95% CI = 0.45-0.77), and 0.65 (95% CI = 0.46-0.85), respectively. From the FFPE samples, the 69-gene LDA could discriminate AC responders, with AUC of 0.79 (95% CI = 0.59-0.98). In conclusion, a promising defective DNA repair gene expression signature appears to differentiate TN breast cancers that are sensitive to anthracyclines and resistant to taxane-based chemotherapy, and should be tested in clinical trials with other DNA-damaging agents and PARP-1 inhibitors. AD - Dan L Duncan Cancer Center, Baylor College of Medicine, 1 Baylor Plaza BCM 600, Houston, TX 77030, USA. FAU - Rodriguez, A A AU - Rodriguez AA FAU - Makris, A AU - Makris A FAU - Wu, M F AU - Wu MF FAU - Rimawi, M AU - Rimawi M FAU - Froehlich, A AU - Froehlich A FAU - Dave, B AU - Dave B FAU - Hilsenbeck, S G AU - Hilsenbeck SG FAU - Chamness, G C AU - Chamness GC FAU - Lewis, M T AU - Lewis MT FAU - Dobrolecki, L E AU - Dobrolecki LE FAU - Jain, D AU - Jain D FAU - Sahoo, S AU - Sahoo S FAU - Osborne, C K AU - Osborne CK FAU - Chang, J C AU - Chang JC LA - eng PT - Journal Article DEP - 20100626 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Anthracyclines) RN - 0 (Antineoplastic Agents) RN - 0 (FEC protocol) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Taxoids) RN - 50-18-0 (Cyclophosphamide) RN - 51-21-8 (Fluorouracil) RN - 56420-45-2 (Epirubicin) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Anthracyclines/*therapeutic use MH - Antineoplastic Agents/therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/therapeutic use MH - Area Under Curve MH - Breast Neoplasms/*drug therapy/*genetics MH - Clinical Trials as Topic MH - Cyclophosphamide/therapeutic use MH - DNA Repair/*genetics MH - Drug Resistance, Neoplasm/*genetics MH - Epirubicin/therapeutic use MH - Female MH - Fluorouracil/therapeutic use MH - Gene Expression Profiling MH - Humans MH - Neoadjuvant Therapy MH - Oligonucleotide Array Sequence Analysis MH - Prognosis MH - ROC Curve MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics MH - Reverse Transcriptase Polymerase Chain Reaction MH - Taxoids/therapeutic use EDAT- 2010/06/29 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/06/29 06:00 PHST- 2010/05/31 [received] PHST- 2010/06/04 [accepted] PHST- 2010/06/26 [aheadofprint] AID - 10.1007/s10549-010-0983-z [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):189-96. Epub 2010 Jun 26. PMID- 20579331 OWN - NLM STAT- MEDLINE DA - 20100730 DCOM- 20101028 IS - 1756-9966 (Electronic) IS - 0392-9078 (Linking) VI - 29 DP - 2010 TI - Presymptomatic breast cancer in Egypt: role of BRCA1 and BRCA2 tumor suppressor genes mutations detection. PG - 82 AB - BACKGROUND: Breast cancer is one of the most common diseases affecting women. Inherited susceptibility genes, BRCA1 and BRCA2, are considered in breast, ovarian and other common cancers etiology. BRCA1 and BRCA2 genes have been identified that confer a high degree of breast cancer risk. OBJECTIVE: Our study was performed to identify germline mutations in some exons of BRCA1 and BRCA2 genes for the early detection of presymptomatic breast cancer in females. METHODS: This study was applied on Egyptian healthy females who first degree relatives to those, with or without a family history, infected with breast cancer. Sixty breast cancer patients, derived from 60 families, were selected for molecular genetic testing of BRCA1 and BRCA2 genes. The study also included 120 healthy first degree female relatives of the patients, either sisters and/or daughters, for early detection of presymptomatic breast cancer mutation carriers. Genomic DNA was extracted from peripheral blood lymphocytes of all the studied subjects. Universal primers were used to amplify four regions of the BRCA1 gene (exons 2,8,13 and 22) and one region (exon 9) of BRCA2 gene using specific PCR. The polymerase chain reaction was carried out. Single strand conformation polymorphism assay and heteroduplex analysis were used to screen for mutations in the studied exons. In addition, DNA sequencing of the normal and mutated exons were performed. RESULTS: Mutations in both BRCA1 and BRCA2 genes were detected in 86.7% of the families. Current study indicates that 60% of these families were attributable to BRCA1 mutations, while 26.7% of them were attributable to BRCA2 mutations. Results showed that four mutations were detected in the BRCA1 gene, while one mutation was detected in the BRCA2 gene. Asymptomatic relatives, 80 (67%) out of total 120, were mutation carriers. CONCLUSIONS: BRCA1 and BRCA2 genes mutations are responsible for a significant proportion of breast cancer. BRCA mutations were found in individuals with and without family history. AD - Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt. safinazsibrahim@cu.edu.eg FAU - Ibrahim, Safinaz S AU - Ibrahim SS FAU - Hafez, Elsayed E AU - Hafez EE FAU - Hashishe, Mervat M AU - Hashishe MM LA - eng PT - Journal Article DEP - 20100625 PL - England TA - J Exp Clin Cancer Res JT - Journal of experimental & clinical cancer research : CR JID - 8308647 RN - 0 (BRCA1 Protein) RN - 0 (BRCA2 Protein) RN - 0 (DNA, Neoplasm) SB - IM MH - Adult MH - BRCA1 Protein/*genetics MH - BRCA2 Protein/*genetics MH - Breast Neoplasms/epidemiology/*genetics/pathology MH - DNA, Neoplasm/genetics MH - Egypt/epidemiology MH - Family MH - Female MH - Germ-Line Mutation/*genetics MH - Humans MH - Male MH - Middle Aged MH - Pedigree MH - Polymerase Chain Reaction MH - Polymorphism, Single-Stranded Conformational MH - Prognosis MH - Young Adult PMC - PMC2912271 OID - NLM: PMC2912271 EDAT- 2010/06/29 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/06/29 06:00 PHST- 2010/04/14 [received] PHST- 2010/06/25 [accepted] PHST- 2010/06/25 [aheadofprint] AID - 1756-9966-29-82 [pii] AID - 10.1186/1756-9966-29-82 [doi] PST - epublish SO - J Exp Clin Cancer Res. 2010 Jun 25;29:82. PMID- 20576095 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Genomic subtypes of breast cancer identified by array-comparative genomic hybridization display distinct molecular and clinical characteristics. PG - R42 AB - INTRODUCTION: Breast cancer is a profoundly heterogeneous disease with respect to biologic and clinical behavior. Gene-expression profiling has been used to dissect this complexity and to stratify tumors into intrinsic gene-expression subtypes, associated with distinct biology, patient outcome, and genomic alterations. Additionally, breast tumors occurring in individuals with germline BRCA1 or BRCA2 mutations typically fall into distinct subtypes. METHODS: We applied global DNA copy number and gene-expression profiling in 359 breast tumors. All tumors were classified according to intrinsic gene-expression subtypes and included cases from genetically predisposed women. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was used to identify significant DNA copy-number aberrations and genomic subgroups of breast cancer. RESULTS: We identified 31 genomic regions that were highly amplified in > 1% of the 359 breast tumors. Several amplicons were found to co-occur, the 8p12 and 11q13.3 regions being the most frequent combination besides amplicons on the same chromosomal arm. Unsupervised hierarchical clustering with 133 significant GISTIC regions revealed six genomic subtypes, termed 17q12, basal-complex, luminal-simple, luminal-complex, amplifier, and mixed subtypes. Four of them had striking similarity to intrinsic gene-expression subtypes and showed associations to conventional tumor biomarkers and clinical outcome. However, luminal A-classified tumors were distributed in two main genomic subtypes, luminal-simple and luminal-complex, the former group having a better prognosis, whereas the latter group included also luminal B and the majority of BRCA2-mutated tumors. The basal-complex subtype displayed extensive genomic homogeneity and harbored the majority of BRCA1-mutated tumors. The 17q12 subtype comprised mostly HER2-amplified and HER2-enriched subtype tumors and had the worst prognosis. The amplifier and mixed subtypes contained tumors from all gene-expression subtypes, the former being enriched for 8p12-amplified cases, whereas the mixed subtype included many tumors with predominantly DNA copy-number losses and poor prognosis. CONCLUSIONS: Global DNA copy-number analysis integrated with gene-expression data can be used to dissect the complexity of breast cancer. This revealed six genomic subtypes with different clinical behavior and a striking concordance to the intrinsic subtypes. These genomic subtypes may prove useful for understanding the mechanisms of tumor development and for prognostic and treatment prediction purposes. AD - Department of Oncology, Clinical Sciences, Lund University and Skane University Hospital, Barngatan 2B, 5 Lund, Sweden. goran_b.jonsson@med.lu.se FAU - Jonsson, Goran AU - Jonsson G FAU - Staaf, Johan AU - Staaf J FAU - Vallon-Christersson, Johan AU - Vallon-Christersson J FAU - Ringner, Markus AU - Ringner M FAU - Holm, Karolina AU - Holm K FAU - Hegardt, Cecilia AU - Hegardt C FAU - Gunnarsson, Haukur AU - Gunnarsson H FAU - Fagerholm, Rainer AU - Fagerholm R FAU - Strand, Carina AU - Strand C FAU - Agnarsson, Bjarni A AU - Agnarsson BA FAU - Kilpivaara, Outi AU - Kilpivaara O FAU - Luts, Lena AU - Luts L FAU - Heikkila, Paivi AU - Heikkila P FAU - Aittomaki, Kristiina AU - Aittomaki K FAU - Blomqvist, Carl AU - Blomqvist C FAU - Loman, Niklas AU - Loman N FAU - Malmstrom, Per AU - Malmstrom P FAU - Olsson, Hakan AU - Olsson H FAU - Johannsson, Oskar Th AU - Johannsson OT FAU - Arason, Adalgeir AU - Arason A FAU - Nevanlinna, Heli AU - Nevanlinna H FAU - Barkardottir, Rosa B AU - Barkardottir RB FAU - Borg, Ake AU - Borg A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100624 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (BRCA1 Protein) RN - 0 (BRCA2 Protein) RN - 0 (Tumor Markers, Biological) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - BRCA1 Protein/genetics MH - BRCA2 Protein/genetics MH - Breast Neoplasms/*classification/*genetics/pathology MH - *Comparative Genomic Hybridization MH - Female MH - Follow-Up Studies MH - *Gene Expression Profiling MH - Genetic Predisposition to Disease MH - Humans MH - Middle Aged MH - Mutation/genetics MH - Neoplasms, Basal Cell/*classification/*genetics/pathology MH - Oligonucleotide Array Sequence Analysis MH - Prognosis MH - Survival Rate MH - Tumor Markers, Biological/genetics/metabolism PMC - PMC2917037 OID - NLM: PMC2917037 EDAT- 2010/06/26 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/26 06:00 PHST- 2009/12/15 [received] PHST- 2010/05/18 [revised] PHST- 2010/06/24 [accepted] PHST- 2010/06/24 [aheadofprint] AID - bcr2596 [pii] AID - 10.1186/bcr2596 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R42. Epub 2010 Jun 24. PMID- 20574671 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Triple negative breast cancer in Korea-distinct biology with different impact of prognostic factors on survival. PG - 177-87 AB - We analyzed breast cancer subtypes using Korean Breast Cancer Society Registration Program data to compare clinical features and prognosis for triple-negative breast cancer (TNBC). A cohort of 26,767 breast cancer patients were divided in four groups: luminal A (ER+ and/or PR+, HER2-), luminal B (ER+ and/or PR+ HER2+), HER2+ (ER-, PR-, HER2+), and triple-negative (ER-, PR-, HER2-). Clinicopathologic factors were evaluated. The luminal A (14,437 patients, 53.9%) subtype was the largest in our study. Compared with luminal A subtype, TNBC correlated with younger age, more aggressive characteristics and poor overall survival and breast cancer-specific survival. The hazard rate showed a peak at 24 months for the TNBC subtype, but after 60 months, risk was similar to that of the luminal A subtype. Higher T, N stage and histologic grade, and lymphatic and vascular invasion showed poor prognosis in TNBC patients, but on multivariate analysis only histologic grade and ki-67 status were related. Young age was related to poor prognosis in the luminal A subtype, however, age was not related to prognosis in the TNBC subtype. Of the 5,586 TNBC patients, 282 patients (7.11%) expired within 3 years of diagnosis. T and N stage and grade were significantly associated with prognosis on multivariate analysis. TNBC subtype is characterized by younger age with poorer outcome. However, younger age is not related to prognosis, and mortality risk decreases to that of the luminal A subtype, which is known to have the best prognosis after a few years. AD - Department of General Surgery, Anam Hospital, Korea University, College of Medicine, 126-, Anam-dong 5-ga, Seongbuk-gu, Seoul 136-705, Korea. FAU - Lee, Jung Ah AU - Lee JA FAU - Kim, Kwan-Il AU - Kim KI FAU - Bae, Jeoung Won AU - Bae JW FAU - Jung, Young-Hoon AU - Jung YH FAU - An, Hyonggin AU - An H FAU - Lee, Eun Sook AU - Lee ES CN - Korean Breast Cancer Society LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100624 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Markers, Biological) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Adult MH - Age Factors MH - Breast Neoplasms/*genetics/*mortality/*pathology MH - Female MH - Humans MH - Kaplan-Meiers Estimate MH - Korea MH - Middle Aged MH - Neoplasm Staging MH - Prognosis MH - Proportional Hazards Models MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics MH - Registries MH - Retrospective Studies MH - Tumor Markers, Biological/*analysis IR - Ahn SH FIR - Ahn, S H IR - Bae JW FIR - Bae, J W IR - Bae YT FIR - Bae, Y T IR - Baek JW FIR - Baek, J W IR - Bong JG FIR - Bong, J G IR - Cha KH FIR - Cha, K H IR - Chang ES FIR - Chang, E S IR - Chang IT FIR - Chang, I T IR - Chang SS FIR - Chang, S S IR - Cho JW FIR - Cho, J W IR - Cho SH FIR - Cho, S H IR - Cho YU FIR - Cho, Y U IR - Choi JW FIR - Choi, J W IR - Choi KJ FIR - Choi, K J IR - Choi MS FIR - Choi, M S IR - Choi SI FIR - Choi, S I IR - Choi SY FIR - Choi, S Y IR - Goo GS FIR - Goo, G S IR - Han SH FIR - Han, S H IR - Han W FIR - Han, W IR - Hong SJ FIR - Hong, S J IR - Hwang JY FIR - Hwang, J Y IR - Hyun TI FIR - Hyun, T I IR - Jegal YJ FIR - Jegal, Y J IR - Im MG FIR - Im, M G IR - Joh YG FIR - Joh, Y G IR - Jun SY FIR - Jun, S Y IR - Jung BW FIR - Jung, B W IR - Jung J FIR - Jung, J IR - Jung JH FIR - Jung, J H IR - Jung KH FIR - Jung, K H IR - Jung PJ FIR - Jung, P J IR - Jung SH FIR - Jung, S H IR - Jung SS FIR - Jung, S S IR - Jung YH FIR - Jung, Y H IR - Jung YS FIR - Jung, Y S IR - Kang DH FIR - Kang, D H IR - Kang HJ FIR - Kang, H J IR - Kang YI FIR - Kang, Y I IR - Kang YJ FIR - Kang, Y J IR - Keum JH FIR - Keum, J H IR - Kim DY FIR - Kim, D Y IR - Kim HJ FIR - Kim, H J IR - Kim JG FIR - Kim, J G IR - Kim JH FIR - Kim, J H IR - Kim JS FIR - Kim, J S IR - Kim JS FIR - Kim, J S IR - Kim KC FIR - Kim, K C IR - Kim SC FIR - Kim, S C IR - Kim SH FIR - Kim, S H IR - Kim SI FIR - Kim, S I IR - Kim SJ FIR - Kim, S J IR - Kim SW FIR - Kim, S W IR - Kim SW FIR - Kim, S W IR - Kim SY FIR - Kim, S Y IR - Kim SY FIR - Kim, S Y IR - Kim YS FIR - Kim, Y S IR - Ko BK FIR - Ko, B K IR - Ko SS FIR - Ko, S S IR - Koh SH FIR - Koh, S H IR - Koo BH FIR - Koo, B H IR - Koo JY FIR - Koo, J Y IR - Kwak BS FIR - Kwak, B S IR - Lee CH FIR - Lee, C H IR - Lee CH FIR - Lee, C H IR - Lee DH FIR - Lee, D H IR - Lee DS FIR - Lee, D S IR - Lee ES FIR - Lee, E S IR - Lee GS FIR - Lee, G S IR - Lee HD FIR - Lee, H D IR - Lee HS FIR - Lee, H S IR - Lee JC FIR - Lee, J C IR - Lee JH FIR - Lee, J H IR - Lee JK FIR - Lee, J K IR - Lee JS FIR - Lee, J S IR - Lee JY FIR - Lee, J Y IR - Lee KM FIR - Lee, K M IR - Lee KP FIR - Lee, K P IR - Lee KS FIR - Lee, K S IR - Lee KY FIR - Lee, K Y IR - Lee MH FIR - Lee, M H IR - Lee RA FIR - Lee, R A IR - Lee SC FIR - Lee, S C IR - Lee SJ FIR - Lee, S J IR - Lee SK FIR - Lee, S K IR - Lee W FIR - Lee, W IR - Lee YH FIR - Lee, Y H IR - Leu JW FIR - Leu, J W IR - Lim CH FIR - Lim, C H IR - Lim CW FIR - Lim, C W IR - Moon BI FIR - Moon, B I IR - Nam YS FIR - Nam, Y S IR - Nam SJ FIR - Nam, S J IR - Noh DY FIR - Noh, D Y IR - Noh WC FIR - Noh, W C IR - Oh SJ FIR - Oh, S J IR - Oh SS FIR - Oh, S S IR - Pae WK FIR - Pae, W K IR - Paik IW FIR - Paik, I W IR - Paik NS FIR - Paik, N S IR - Park BG FIR - Park, B G IR - Park BW FIR - Park, B W IR - Park CH FIR - Park, C H IR - Park HB FIR - Park, H B IR - Park HY FIR - Park, H Y IR - Park JH FIR - Park, J H IR - Park KH FIR - Park, K H IR - Park SJ FIR - Park, S J IR - Park ST FIR - Park, S T IR - Park SW FIR - Park, S W IR - Park WC FIR - Park, W C IR - Park YK FIR - Park, Y K IR - Park YK FIR - Park, Y K IR - Seo HS FIR - Seo, H S IR - Seo KH FIR - Seo, K H IR - Seo YJ FIR - Seo, Y J IR - Sin YS FIR - Sin, Y S IR - Son BH FIR - Son, B H IR - Son GS FIR - Son, G S IR - Song BJ FIR - Song, B J IR - Song KH FIR - Song, K H IR - Song YJ FIR - Song, Y J IR - Suh YJ FIR - Suh, Y J IR - Won JM FIR - Won, J M IR - Woo DH FIR - Woo, D H IR - Yang DH FIR - Yang, D H IR - Yang JH FIR - Yang, J H IR - Yoo KY FIR - Yoo, K Y IR - Yoo SY FIR - Yoo, S Y IR - Yoon HS FIR - Yoon, H S IR - Yoon JH FIR - Yoon, J H IR - Yoon SO FIR - Yoon, S O EDAT- 2010/06/25 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/06/25 06:00 PHST- 2010/05/03 [received] PHST- 2010/06/11 [accepted] PHST- 2010/06/24 [aheadofprint] AID - 10.1007/s10549-010-0998-5 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):177-87. Epub 2010 Jun 24. PMID- 20570914 OWN - NLM STAT- MEDLINE DA - 20100709 DCOM- 20101028 IS - 1538-7755 (Electronic) IS - 1055-9965 (Linking) VI - 19 IP - 7 DP - 2010 Jul TI - Timing of menarche and first birth in relation to risk of breast cancer in A-bomb survivors. PG - 1746-54 AB - BACKGROUND: The length of the interval between age at menarche and age at first birth is positively associated with breast cancer risk. We examined the risk of breast cancer in atomic bomb survivors to investigate whether women exposed to radiation between menarche and first birth had a higher risk of radiogenic breast cancer than women exposed at the same age but outside this interval. METHODS: Women (n = 30,113) were classified into three reproductive status at the time of the bombings (ATB) categories (premenarche, between menarche and first birth, or after first birth). Poisson regression was used to test the primary hypothesis. RESULTS: When the background rate of breast cancer was taken to depend on city, age ATB, and attained age only, the radiation-related excess relative risk (ERR) varied significantly among the three categories (P = 0.049). However, after controlling for significant heterogeneity in the baseline risk of breast cancer between reproductive status ATB groups (P < 0.001), no significant heterogeneity (P = 0.88) was observed in the ERR, with an ERR per Gy of 1.36 [95% confidence interval (CI), 0.54-2.75] for women exposed between menarche and first birth ATB, and 1.07 (95% CI, 0.22-3.62) and 1.53 (95% CI, 0.63-2.90) for those exposed premenarche or after first birth, respectively. CONCLUSIONS: The radiation-associated risk of breast cancer does not vary significantly by reproductive status ATB. IMPACT: It is possible that radiation exerts similar carcinogenic effects on the breast regardless of its stage of differentiation, or that the differences in radiosensitivity are too small to be detected in this cohort. AD - Department of Epidemiology, University of Washington, Health Sciences F-263, Box 357236, Seattle, WA 98195-7236, USA. mcdouj@u.washington.edu FAU - McDougall, Jean A AU - McDougall JA FAU - Sakata, Ritsu AU - Sakata R FAU - Sugiyama, Hiromi AU - Sugiyama H FAU - Grant, Eric AU - Grant E FAU - Davis, Scott AU - Davis S FAU - Nishi, Nobuo AU - Nishi N FAU - Soda, Midori AU - Soda M FAU - Shimizu, Yukiko AU - Shimizu Y FAU - Tatsukawa, Yoshimi AU - Tatsukawa Y FAU - Kasagi, Fumiyoshi AU - Kasagi F FAU - Suyama, Akihiko AU - Suyama A FAU - Ross, Phillip AU - Ross P FAU - Kopecky, Kenneth J AU - Kopecky KJ FAU - Li, Christopher I AU - Li CI LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. DEP - 20100622 PL - United States TA - Cancer Epidemiol Biomarkers Prev JT - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JID - 9200608 SB - IM MH - Age Factors MH - Breast Neoplasms/*epidemiology/etiology MH - Cohort Studies MH - Female MH - Humans MH - Incidence MH - Japan/epidemiology MH - *Menarche MH - Neoplasms, Radiation-Induced/*epidemiology MH - *Nuclear Warfare MH - Pregnancy MH - Radiation Dosage MH - Reproductive History MH - Risk Factors MH - Survivors/*statistics & numerical data EDAT- 2010/06/24 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/06/24 06:00 PHST- 2010/06/22 [aheadofprint] AID - 1055-9965.EPI-10-0246 [pii] AID - 10.1158/1055-9965.EPI-10-0246 [doi] PST - ppublish SO - Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1746-54. Epub 2010 Jun 22. PMID- 20570912 OWN - NLM STAT- MEDLINE DA - 20100709 DCOM- 20101028 IS - 1538-7755 (Electronic) IS - 1055-9965 (Linking) VI - 19 IP - 7 DP - 2010 Jul TI - No association between TERT-CLPTM1L single nucleotide polymorphism rs401681 and mean telomere length or cancer risk. PG - 1862-5 AB - BACKGROUND: A recent study reported genetic variants in the TERT-CLPTM1L locus that were associated with mean telomere length, and with risk of multiple cancers. METHODS: We evaluated the association between single nucleotide polymorphism (SNP) rs401681 (C > T) and mean telomere length, using quantitative real-time PCR, in blood-extracted DNA collected from 11,314 cancer-free participants from the Sisters in Breast Screening study, the Melanoma and Pigmented Lesions Evaluative Study melanoma family study, and the SEARCH Breast, Colorectal, Melanoma studies. We also examined the relationship between rs401618 genotype and susceptibility to breast cancer (6,800 cases and 6,608 controls), colorectal cancer (2,259 cases and 2,181 controls), and melanoma (787 cases and 999 controls). RESULTS: The "per T allele" change in mean telomere length (DeltaCt), adjusted for age, study plate, gender, and family was 0.001 [95% confidence intervals (CI), 0.01-0.02; P trend = 0.61]. The "per T allele" odds ratio for each cancer was 1.01 for breast cancer (95% CI, 0.96-1.06; P trend = 0.64), 1.02 for colorectal cancer (95% CI, 0.94-1.11; P trend = 0.66), and 0.99 for melanoma (95% CI, 0.84-1.15; P trend = 0.87). CONCLUSIONS: We found no evidence that this SNP was associated with mean telomere length, or with risk of breast cancer, colorectal cancer, or melanoma. IMPACT: Our results indicate that the observed associations between rs401681 and several cancer types might be weaker than previously described. The lack of an association in our study between this SNP and mean telomere length suggests that any association with cancer risk at this locus is not mediated through TERT. AD - Cancer Research UK Genetic Epidemiology Unit, Department of Public Health and Primary Care, Strangeways Research Laboratory, 2 Worts Causeway, Cambridge CB18RN, United Kingdom. karen.pooley@srl.cam.ac.uk FAU - Pooley, Karen A AU - Pooley KA FAU - Tyrer, Jonathan AU - Tyrer J FAU - Shah, Mitul AU - Shah M FAU - Driver, Kristy E AU - Driver KE FAU - Leyland, Jean AU - Leyland J FAU - Brown, Judith AU - Brown J FAU - Audley, Tina AU - Audley T FAU - McGuffog, Lesley AU - McGuffog L FAU - Ponder, Bruce A J AU - Ponder BA FAU - Pharoah, Paul D P AU - Pharoah PD FAU - Easton, Douglas F AU - Easton DF FAU - Dunning, Alison M AU - Dunning AM LA - eng GR - A10119/Cancer Research UK/United Kingdom GR - A10123/Cancer Research UK/United Kingdom GR - A10124/Cancer Research UK/United Kingdom PT - Journal Article DEP - 20100622 PL - United States TA - Cancer Epidemiol Biomarkers Prev JT - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology JID - 9200608 RN - 0 (CLPTM1L protein, human) RN - 0 (Membrane Proteins) RN - 0 (Neoplasm Proteins) RN - 0 (Tumor Markers, Biological) RN - EC 2.7.7.49 (TERT protein, human) RN - EC 2.7.7.49 (Telomerase) SB - IM MH - Adolescent MH - Adult MH - Aged MH - Aged, 80 and over MH - Breast Neoplasms/enzymology/genetics MH - Case-Control Studies MH - Colorectal Neoplasms/enzymology/genetics MH - Female MH - Genetic Predisposition to Disease MH - Genetic Variation MH - Humans MH - Male MH - Melanoma/enzymology/genetics MH - Membrane Proteins/*genetics MH - Middle Aged MH - Neoplasm Proteins/*genetics MH - Neoplasms/enzymology/*genetics MH - Polymorphism, Single Nucleotide MH - Risk Factors MH - Telomerase/*genetics MH - Telomere/chemistry/*genetics/pathology MH - Tumor Markers, Biological MH - Young Adult PMC - PMC2901592 MID - UKMS29927 OID - NLM: PMC2901592 [Available on 01/01/11] OID - NLM: UKMS29927 [Available on 01/01/11] EDAT- 2010/06/24 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/06/24 06:00 PMCR- 2011/01/01 PHST- 2010/06/22 [aheadofprint] AID - 1055-9965.EPI-10-0281 [pii] AID - 10.1158/1055-9965.EPI-10-0281 [doi] PST - ppublish SO - Cancer Epidemiol Biomarkers Prev. 2010 Jul;19(7):1862-5. Epub 2010 Jun 22. PMID- 20568049 OWN - NLM STAT- MEDLINE DA - 20100622 DCOM- 20101105 IS - 1676-5680 (Electronic) IS - 1676-5680 (Linking) VI - 9 IP - 2 DP - 2010 TI - GSTT1, GSTM1, and GSTP1 polymorphisms and chemotherapy response in locally advanced breast cancer. PG - 1045-53 AB - The glutathione S-transferase (GST) family consists of phase II detoxification enzymes that catalyze the conjugation of toxic substances, such as chemotherapeutic agents, to glutathione. We examined whether GSTT1/GSTT1"null", GSTM1/GSTM1"null" and GSTP1Ile105Ile/GSTP1Ile105Val polymorphisms are associated with different response rates to neoadjuvant chemotherapy in the treatment of stage II and III breast cancer. Forty Brazilian women with invasive ductal adenocarcinoma of the breast submitted to neoadjuvant chemotherapy, using 5-fluorouracil, epirubicin and cyclophosphamide, were genotyped for the GSTT1, GSTM1 and GSTP1 genes. Clinical response was assessed by RECIST criteria. Comparisons were made for the three genes alone and in pairs, as polymorphic and as wild-type combinations and polymorphic/wild-type combinations. We analyzed all possible combinations and their response rate. Patients with the GSTT1/GSTP1105Ile combination were found to have a significantly better response than GSTT1"null"/GSTP1105Val (P = 0.0209) and GSTT1/GSTM1 (P = 0.0376) combinations. Analysis of all possible combinations showed the GSTM1"null" polymorphic genotype to be present in four, and the wild-type GSTP1105Ile in six of the combinations associated with the largest number of responding patients. We found that patients with the GSTT1/GSTP1105Ile wild-type combination had a significantly higher response rate to chemotherapy than patients with the respective polymorphic GSTT1"null"/GSTP1105Val combination or patients with the wild-type GSTT1/GSTM1. The six gene combinations associated with the largest number of responding patients were found to contain the wild-type GSTP1105Ile and the polymorphic-type GSTM1"null". These specific combinations were virtually absent in the combinations with few responding patients. AD - Departamento de Ginecologia e Obstetricia, Irmandade da Santa Casa de Misericordia de Sao Paulo, Faculdade de Ciencias Medicas, Sao Paulo, SP, Brasil. drandrel@terra.com.br FAU - Oliveira, A L AU - Oliveira AL FAU - Rodrigues, F F O AU - Rodrigues FF FAU - Santos, R E AU - Santos RE FAU - Aoki, T AU - Aoki T FAU - Rocha, M N AU - Rocha MN FAU - Longui, C A AU - Longui CA FAU - Melo, M B AU - Melo MB LA - eng PT - Journal Article DEP - 20100611 PL - Brazil TA - Genet Mol Res JT - Genetics and molecular research : GMR JID - 101169387 RN - 0 (Antineoplastic Agents) RN - 50-18-0 (Cyclophosphamide) RN - 51-21-8 (Fluorouracil) RN - 56420-45-2 (Epirubicin) RN - 70-18-8 (Glutathione) RN - EC 2.5.1.- (glutathione S-transferase T1) RN - EC 2.5.1.18 (GSTP1 protein, human) RN - EC 2.5.1.18 (Glutathione S-Transferase pi) RN - EC 2.5.1.18 (Glutathione Transferase) RN - EC 2.5.1.18 (glutathione S-transferase M1) SB - IM MH - Adult MH - Aged MH - Antineoplastic Agents/*therapeutic use MH - Brazil MH - Breast Neoplasms/*drug therapy/enzymology/*genetics MH - Carcinoma, Ductal, Breast/genetics MH - Cyclophosphamide/therapeutic use MH - Epirubicin/therapeutic use MH - Female MH - Fluorouracil/therapeutic use MH - Glutathione/metabolism MH - Glutathione S-Transferase pi/*genetics MH - Glutathione Transferase/*genetics MH - Humans MH - Middle Aged MH - *Polymorphism, Genetic MH - Treatment Outcome EDAT- 2010/06/23 06:00 MHDA- 2010/11/06 06:00 CRDT- 2010/06/23 06:00 AID - gmr726 [pii] AID - 10.4238/vol9-2gmr726 [doi] PST - epublish SO - Genet Mol Res. 2010 Jun 11;9(2):1045-53. PMID- 20567162 OWN - NLM STAT- MEDLINE DA - 20100622 DCOM- 20101115 IS - 1873-233X (Electronic) IS - 0029-7844 (Linking) VI - 116 IP - 1 DP - 2010 Jul TI - Waiting for the tide to change: reducing risk in the turbulent sea of liability. PG - 8-15 AD - james.shwayder@louisville.edu FAU - Shwayder, James M AU - Shwayder JM LA - eng PT - Journal Article PL - United States TA - Obstet Gynecol JT - Obstetrics and gynecology JID - 0401101 RN - 0 (Oxytocics) RN - 50-56-6 (Oxytocin) SB - AIM SB - IM MH - Attitude of Health Personnel MH - Birth Injuries MH - Breast Neoplasms/diagnosis MH - Cesarean Section MH - Female MH - Gynecology/*trends MH - Humans MH - Infant, Newborn MH - *Liability, Legal MH - Obstetric Labor Complications MH - Obstetrics/*trends MH - Oxytocics/adverse effects MH - Oxytocin/adverse effects MH - Pregnancy MH - United States EDAT- 2010/06/23 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/23 06:00 AID - 10.1097/AOG.0b013e3181e5e2ec [doi] AID - 00006250-201007000-00005 [pii] PST - ppublish SO - Obstet Gynecol. 2010 Jul;116(1):8-15. PMID- 20565864 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Molecular subtypes of breast cancer are associated with characteristic DNA methylation patterns. PG - R36 AB - INTRODUCTION: Five different molecular subtypes of breast cancer have been identified through gene expression profiling. Each subtype has a characteristic expression pattern suggested to partly depend on cellular origin. We aimed to investigate whether the molecular subtypes also display distinct methylation profiles. METHODS: We analysed methylation status of 807 cancer-related genes in 189 fresh frozen primary breast tumours and four normal breast tissue samples using an array-based methylation assay. RESULTS: Unsupervised analysis revealed three groups of breast cancer with characteristic methylation patterns. The three groups were associated with the luminal A, luminal B and basal-like molecular subtypes of breast cancer, respectively, whereas cancers of the HER2-enriched and normal-like subtypes were distributed among the three groups. The methylation frequencies were significantly different between subtypes, with luminal B and basal-like tumours being most and least frequently methylated, respectively. Moreover, targets of the polycomb repressor complex in breast cancer and embryonic stem cells were more methylated in luminal B tumours than in other tumours. BRCA2-mutated tumours had a particularly high degree of methylation. Finally, by utilizing gene expression data, we observed that a large fraction of genes reported as having subtype-specific expression patterns might be regulated through methylation. CONCLUSIONS: We have found that breast cancers of the basal-like, luminal A and luminal B molecular subtypes harbour specific methylation profiles. Our results suggest that methylation may play an important role in the development of breast cancers. AD - Department of Oncology, Clinical Sciences, Lund University, Barngatan 2B, Lund, Sweden. karolina.holm@med.lu.se FAU - Holm, Karolina AU - Holm K FAU - Hegardt, Cecilia AU - Hegardt C FAU - Staaf, Johan AU - Staaf J FAU - Vallon-Christersson, Johan AU - Vallon-Christersson J FAU - Jonsson, Goran AU - Jonsson G FAU - Olsson, Hakan AU - Olsson H FAU - Borg, Ake AU - Borg A FAU - Ringner, Markus AU - Ringner M LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100618 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (DNA, Neoplasm) SB - IM MH - Breast/*metabolism/pathology MH - Breast Neoplasms/*classification/*genetics/pathology MH - CpG Islands MH - *DNA Methylation MH - DNA, Neoplasm/genetics MH - Female MH - Gene Dosage MH - Genes, BRCA1 MH - Genes, BRCA2 MH - Humans MH - Middle Aged MH - Mutation/genetics MH - Neoplasms, Basal Cell/*classification/*genetics/pathology MH - Oligonucleotide Array Sequence Analysis MH - Polymerase Chain Reaction MH - Prognosis MH - Promoter Regions, Genetic/genetics MH - Survival Rate PMC - PMC2917031 OID - NLM: PMC2917031 EDAT- 2010/06/23 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/23 06:00 PHST- 2009/11/19 [received] PHST- 2010/05/21 [revised] PHST- 2010/06/18 [accepted] PHST- 2010/06/18 [aheadofprint] AID - bcr2590 [pii] AID - 10.1186/bcr2590 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R36. Epub 2010 Jun 18. PMID- 20565829 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Pregnancy-related factors and the risk of breast carcinoma in situ and invasive breast cancer among postmenopausal women in the California Teachers Study cohort. PG - R35 AB - INTRODUCTION: Although pregnancy-related factors such as nulliparity and late age at first full-term pregnancy are well-established risk factors for invasive breast cancer, the roles of these factors in the natural history of breast cancer development remain unclear. METHODS: Among 52,464 postmenopausal women participating in the California Teachers Study (CTS), 624 were diagnosed with breast carcinoma in situ (CIS) and 2,828 with invasive breast cancer between 1995 and 2007. Multivariable Cox proportional hazards regression methods were used to estimate relative risks associated with parity, age at first full-term pregnancy, breastfeeding, nausea or vomiting during pregnancy, and preeclampsia. RESULTS: Compared with never-pregnant women, an increasing number of full-term pregnancies was associated with greater risk reduction for both breast CIS and invasive breast cancer (both P trend < 0.01). Women having four or more full-term pregnancies had a 31% lower breast CIS risk (RR = 0.69, 95% CI = 0.51 to 0.93) and 18% lower invasive breast cancer risk (RR = 0.82, 95% CI = 0.72 to 0.94). Parous women whose first full-term pregnancy occurred at age 35 years or later had a 118% greater risk for breast CIS (RR = 2.18, 95% CI = 1.36 to 3.49) and 27% greater risk for invasive breast cancer (RR = 1.27, 95% CI = 0.99 to 1.65) than those whose first full-term pregnancy occurred before age 21 years. Furthermore, parity was negatively associated with the risk of estrogen receptor-positive (ER+) or ER+/progesterone receptor-positive (PR+) while age at first full-term pregnancy was positively associated with the risk of ER+ or ER+/PR+ invasive breast cancer. Neither of these factors was statistically significantly associated with the risk of ER-negative (ER-) or ER-/PR- invasive breast cancer, tests for heterogeneity between subtypes did not reach statistical significance. No clear associations were detected for other pregnancy-related factors. CONCLUSIONS: These results provide some epidemiologic evidence that parity and age at first full-term pregnancy are involved in the development of breast cancer among postmenopausal women. The role of these factors in risk of in situ versus invasive, and hormone receptor-positive versus -negative breast cancer merits further exploration. AD - Department of Population Sciences, Beckman Research Institute, City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA. hma@coh.org FAU - Ma, Huiyan AU - Ma H FAU - Henderson, Katherine D AU - Henderson KD FAU - Sullivan-Halley, Jane AU - Sullivan-Halley J FAU - Duan, Lei AU - Duan L FAU - Marshall, Sarah F AU - Marshall SF FAU - Ursin, Giske AU - Ursin G FAU - Horn-Ross, Pamela L AU - Horn-Ross PL FAU - Largent, Joan AU - Largent J FAU - Deapen, Dennis M AU - Deapen DM FAU - Lacey, James V Jr AU - Lacey JV Jr FAU - Bernstein, Leslie AU - Bernstein L LA - eng GR - K05 CA136967/CA/NCI NIH HHS/United States GR - N01-PC-35136/PC/NCI NIH HHS/United States GR - N01-PC-35139/PC/NCI NIH HHS/United States GR - N02-PC-15105/PC/NCI NIH HHS/United States GR - R01 CA77398/CA/NCI NIH HHS/United States GR - U55/CCR921930-02/PHS HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100618 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) SB - IM MH - Adult MH - *Breast Feeding MH - Breast Neoplasms/*epidemiology/metabolism MH - California/epidemiology MH - Carcinoma, Intraductal, Noninfiltrating/*epidemiology/metabolism MH - Female MH - Humans MH - Incidence MH - Neoplasm Invasiveness MH - *Parity MH - *Postmenopause MH - Pregnancy MH - Prognosis MH - Receptors, Estrogen/analysis MH - Receptors, Progesterone/analysis MH - Risk Assessment MH - Risk Factors MH - Young Adult PMC - PMC2917030 OID - NLM: PMC2917030 EDAT- 2010/06/23 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/23 06:00 PHST- 2010/04/01 [received] PHST- 2010/06/02 [revised] PHST- 2010/06/18 [accepted] PHST- 2010/06/18 [aheadofprint] AID - bcr2589 [pii] AID - 10.1186/bcr2589 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R35. Epub 2010 Jun 18. PMID- 20553628 OWN - NLM STAT- MEDLINE DA - 20100721 DCOM- 20101028 IS - 1756-9966 (Electronic) IS - 0392-9078 (Linking) VI - 29 DP - 2010 TI - Association of interleukin-10 gene polymorphisms with breast cancer in a Chinese population. PG - 72 AB - BACKGROUD: Interleukin-10(IL-10) is a multifunctional cytokine with both immunosuppressive and antiangiogenic functions. Polymorphisms in the IL-10 gene promoter genetically determine interindividual differences in IL-10 production. This study was performed to determined whether polymorphisms in the IL-10 gene promoter were associated with breast cancer in a Chinese Han population. METHODS: We genotyped 315 patients with breast cancer and 322 healthy control subjects for -1082A/G, -819T/C and -592A/C single nucleotide polymorphisms in the promoter region of the IL-10 gene by polymerase chain reactionerestriction fragment length polymorphism (PCR-RFLP). RESULTS: There were no significant differences in genotype, allele, or haplotype frequencies in all three loci between patients and healthy controls. Analysis of breast cancer prognostic and predictive factors revealed that the -1082AA genotype was associated with a significantly increased risk of lymph node (LN) involvement (P = 0.041) and larger tumor size (P = 0.039) at the time of diagnosis. Furthermore, in the haplotype analysis of IL-10 gene, we found that patients carrying ATA haplotype were in higher LN involvement (p = 0.022) and higher tumor stage(p = 0.028) of breast cancer at the time of diagnosis compared with others. CONCLUSIONS: Our findings suggest that IL-10 promoter polymorphisms participate in the progression of breast cancer rather than in its initial development in Chinese Han women. AD - Department of Oncology, State Key Discipline of Cell Biology, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, PR China. FAU - Kong, Fanjun AU - Kong F FAU - Liu, Jie AU - Liu J FAU - Liu, Yongheng AU - Liu Y FAU - Song, Bao AU - Song B FAU - Wang, Hualing AU - Wang H FAU - Liu, Wenchao AU - Liu W LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100617 PL - England TA - J Exp Clin Cancer Res JT - Journal of experimental & clinical cancer research : CR JID - 8308647 RN - 0 (Tumor Markers, Biological) RN - 130068-27-8 (Interleukin-10) RN - 9007-49-2 (DNA) SB - IM MH - Alleles MH - Asian Continental Ancestry Group/genetics MH - Breast Neoplasms/epidemiology/*genetics/pathology MH - Case-Control Studies MH - China/epidemiology MH - DNA/blood/genetics MH - Female MH - Genetic Predisposition to Disease MH - Haplotypes MH - Humans MH - Interleukin-10/*genetics MH - Male MH - Middle Aged MH - Polymerase Chain Reaction MH - Polymorphism, Single Nucleotide/*genetics MH - Prognosis MH - Promoter Regions, Genetic/*genetics MH - Risk Factors MH - Tumor Markers, Biological/*genetics PMC - PMC2907337 OID - NLM: PMC2907337 EDAT- 2010/06/18 06:00 MHDA- 2010/10/29 06:00 CRDT- 2010/06/18 06:00 PHST- 2010/04/26 [received] PHST- 2010/06/17 [accepted] PHST- 2010/06/17 [aheadofprint] AID - 1756-9966-29-72 [pii] AID - 10.1186/1756-9966-29-72 [doi] PST - epublish SO - J Exp Clin Cancer Res. 2010 Jun 17;29:72. PMID- 20551037 OWN - NLM STAT- MEDLINE DA - 20100730 DCOM- 20101115 IS - 1078-0432 (Print) IS - 1078-0432 (Linking) VI - 16 IP - 15 DP - 2010 Aug 1 TI - Clinical implications of gene dosage and gene expression patterns in diploid breast carcinoma. PG - 3860-74 AB - PURPOSE: Deregulation of key cellular pathways is fundamental for the survival and expansion of neoplastic cells. In cancer, regulation of gene transcription can be mediated in a variety of ways. The purpose of this study was to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels, and to associate these genomic changes with clinicopathologic parameters. EXPERIMENTAL DESIGN: We screened 97 invasive diploid breast tumors for DNA copy number alterations and changes in transcriptional levels using array comparative genomic hybridization and expression microarrays, respectively. RESULTS: The integrative analysis identified an increase in the overall number of genetic alterations during tumor progression and 15 specific genomic regions with aberrant DNA copy numbers in at least 25% of the patient population, i.e., 1q22, 1q22-q23.1, 1q25.3, 1q32.1, 1q32.1-q32.2, 8q21.2-q21.3, 8q22.3, 8q24.3, and 16p11.2 were recurrently gained, whereas 11q25, 16q21, 16q23.3, and 17p12 were frequently lost (P < 0.01). An examination of the expression patterns of genes mapping within the detected genetic aberrations identified 47 unique genes and 1 Unigene cluster significantly correlated between the DNA and relative mRNA levels. In addition, more malignant tumors with normal gene dosage levels displayed a recurrent overexpression of UBE2C, S100A8, and CBX2, and downregulation of LOC389033, STC2, DNALI1, SCUBE2, NME5, SUSD3, SERPINA11, AZGP1, and PIP. CONCLUSIONS: Taken together, our findings suggest that the dysregulated genes identified here are critical for breast cancer initiation and progression, and could be used as novel therapeutic targets for drug development to complement classical clinicopathologic features. CI - (c) 2010 AACR. AD - Department of Oncology, Institute of Clinical Sciences, and Laboratory of Clinical Pathology and Cytology, Sahlgrenska Academy at University of Gothenburg, Gula straket 2, Gothenburg, Sweden. toshima.parris@oncology.gu.se FAU - Parris, Toshima Z AU - Parris TZ FAU - Danielsson, Anna AU - Danielsson A FAU - Nemes, Szilard AU - Nemes S FAU - Kovacs, Aniko AU - Kovacs A FAU - Delle, Ulla AU - Delle U FAU - Fallenius, Ghita AU - Fallenius G FAU - Mollerstrom, Elin AU - Mollerstrom E FAU - Karlsson, Per AU - Karlsson P FAU - Helou, Khalil AU - Helou K LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100615 PL - United States TA - Clin Cancer Res JT - Clinical cancer research : an official journal of the American Association for Cancer Research JID - 9502500 SB - IM MH - Adult MH - Aged MH - Breast Neoplasms/*genetics/*pathology MH - Carcinoma/*genetics/*pathology MH - Cell Separation MH - Chromosome Aberrations MH - Cluster Analysis MH - Comparative Genomic Hybridization MH - Diploidy MH - Female MH - Flow Cytometry MH - Gene Dosage MH - Gene Expression MH - *Gene Expression Profiling MH - Genes, Neoplasm/genetics MH - Humans MH - In Situ Hybridization, Fluorescence MH - Middle Aged MH - Neoplasm Staging MH - Oligonucleotide Array Sequence Analysis MH - Reverse Transcriptase Polymerase Chain Reaction EDAT- 2010/06/17 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/17 06:00 PHST- 2010/06/15 [aheadofprint] PHST- 2010/07/20 [aheadofprint] AID - 1078-0432.CCR-10-0889 [pii] AID - 10.1158/1078-0432.CCR-10-0889 [doi] PST - ppublish SO - Clin Cancer Res. 2010 Aug 1;16(15):3860-74. Epub 2010 Jun 15. PMID- 20549338 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Adjuvant chemotherapy is not for everyone. PG - 159-62 AD - University of California, San Francisco, San Francisco, CA, USA. chenderson@hendersonmd.org FAU - Henderson, I Craig AU - Henderson IC LA - eng PT - Journal Article DEP - 20100612 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Antineoplastic Agents) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Antineoplastic Agents/*therapeutic use MH - Breast Neoplasms/*drug therapy/*genetics MH - *Chemotherapy, Adjuvant MH - Female MH - Humans MH - Meta-Analysis as Topic MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics EDAT- 2010/06/16 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/06/16 06:00 PHST- 2010/05/18 [received] PHST- 2010/05/19 [accepted] PHST- 2010/06/12 [aheadofprint] AID - 10.1007/s10549-010-0964-2 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):159-62. Epub 2010 Jun 12. PMID- 20549335 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Re-searching anthracycline therapy. PG - 171-5 AD - Sandro Pitigliani Medical Oncology Unit, Department of Oncology, Hospital of Prato, Istituto Toscano Tumori, Piazza Ospedale 2, 59100 Prato, Italy. FAU - Oakman, Catherine AU - Oakman C FAU - Moretti, Erica AU - Moretti E FAU - Di Leo, Angelo AU - Di Leo A LA - eng PT - Comment PT - Journal Article DEP - 20100615 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Anthracyclines) RN - 0 (Antineoplastic Agents) RN - 0 (Tumor Markers, Biological) SB - IM CON - Breast Cancer Res Treat. 2010 Aug;123(1):163-9. PMID: 20464479 MH - Anthracyclines/*therapeutic use MH - Antineoplastic Agents/therapeutic use MH - Breast Neoplasms/*drug therapy/*genetics MH - Clinical Trials as Topic MH - Drug Resistance, Neoplasm/*genetics MH - Female MH - Humans MH - Meta-Analysis as Topic MH - Tumor Markers, Biological/*genetics EDAT- 2010/06/16 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/06/16 06:00 PHST- 2010/05/27 [received] PHST- 2010/06/04 [accepted] PHST- 2010/06/15 [aheadofprint] AID - 10.1007/s10549-010-0985-x [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):171-5. Epub 2010 Jun 15. PMID- 20540734 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Prospectively measured triiodothyronine levels are positively associated with breast cancer risk in postmenopausal women. PG - R33 AB - INTRODUCTION: The potential association between hypo- and hyperthyroid disorders and breast cancer has been investigated in a large number of studies during the last decades without conclusive results. This prospective cohort study investigated prediagnostic levels of thyrotropin (TSH) and triiodothyronine (T3) in relation to breast cancer incidence in pre- and postmenopausal women. METHODS: In the Malmo Preventive Project, 2,696 women had T3 and/or TSH levels measured at baseline. During a mean follow-up of 19.3 years, 173 incident breast cancer cases were retrieved using record linkage with The Swedish Cancer Registry. Quartile cut-points for T3 and TSH were based on the distribution among all women in the study cohort. A Cox's proportional hazards analysis was used to estimate relative risks (RR), with a confidence interval (CI) of 95%. Trends over quartiles of T3 and TSH were calculated considering a P-value < 0.05 as statistically significant. All analyses were repeated for pre- and peri/postmenopausal women separately. RESULTS: Overall there was a statistically significant association between T3 and breast cancer risk, the adjusted RR in the fourth quartile, as compared to the first, was 1.87 (1.12 to 3.14). In postmenopausal women the RRs for the second, third and fourth quartiles, as compared to the first, were 3.26 (0.96 to 11.1), 5.53 (1.65 to 18.6) and 6.87 (2.09 to 22.6), (P-trend: < 0.001). There were no such associations in pre-menopausal women, and no statistically significant interaction between T3 and menopausal status. Also, no statistically significant association was seen between serum TSH and breast cancer. CONCLUSIONS: This is the first prospective study on T3 levels in relation to breast cancer risk. T3 levels in postmenopausal women were positively associated with the risk of breast cancer in a dose-response manner. AD - Department of Surgery, Skane University Hospital Malmo, Malmo, Sweden. Ada.tosovic@med.lu.se FAU - Tosovic, Ada AU - Tosovic A FAU - Bondeson, Anne-Greth AU - Bondeson AG FAU - Bondeson, Lennart AU - Bondeson L FAU - Ericsson, Ulla-Britt AU - Ericsson UB FAU - Malm, Johan AU - Malm J FAU - Manjer, Jonas AU - Manjer J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100611 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 6893-02-3 (Triiodothyronine) RN - 9002-71-5 (Thyrotropin) SB - IM MH - Breast Neoplasms/*blood/pathology MH - Carcinoma, Intraductal, Noninfiltrating/*blood/pathology MH - Cohort Studies MH - Female MH - Follow-Up Studies MH - Humans MH - Incidence MH - Middle Aged MH - Neoplasm Invasiveness MH - Postmenopause/*blood MH - Premenopause/*blood MH - Prognosis MH - Prospective Studies MH - Radioimmunoassay MH - Risk Factors MH - Survival Rate MH - Thyrotropin/blood MH - Triiodothyronine/*blood PMC - PMC2917028 OID - NLM: PMC2917028 EDAT- 2010/06/15 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/15 06:00 PHST- 2009/12/16 [received] PHST- 2010/05/13 [revised] PHST- 2010/06/11 [accepted] PHST- 2010/06/11 [aheadofprint] AID - bcr2587 [pii] AID - 10.1186/bcr2587 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R33. Epub 2010 Jun 11. PMID- 20519027 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - What do we learn from HER2-positive breast cancer genomic profiles? PG - 107 AB - Patients with a tumor presenting amplification of the HER2 gene are currently proposed trastuzumab (herceptin) and this has greatly changed their outcome. However, a number of HER2-positive cancers show intrinsic or acquired resistance to trastuzumab and there are clear indications that they form a heterogeneous group of tumors. A paper in this issue of Breast Cancer Research addresses this heterogeneity at the genomic level. FAU - Theillet, Charles AU - Theillet C LA - eng PT - Comment PT - Editorial DEP - 20100601 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (Tumor Markers, Biological) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CON - Breast Cancer Res. 2010;12(3):R25. PMID: 20459607 MH - Breast Neoplasms/diagnosis/drug therapy/*genetics MH - Drug Resistance, Neoplasm/*genetics MH - Female MH - *Gene Expression Profiling MH - *Genome, Human MH - Humans MH - Prognosis MH - Receptor, erbB-2/*genetics MH - Tumor Markers, Biological/*genetics PMC - PMC2917015 OID - NLM: PMC2917015 [Available on 12/01/10] EDAT- 2010/06/04 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/06/04 06:00 PMCR- 2010/12/01 PHST- 2010/06/01 [aheadofprint] AID - bcr2571 [pii] AID - 10.1186/bcr2571 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):107. Epub 2010 Jun 1. PMID- 20502344 OWN - NLM STAT- MEDLINE DA - 20100730 DCOM- 20101108 IS - 1473-5709 (Electronic) IS - 0959-8278 (Linking) VI - 19 IP - 5 DP - 2010 Sep TI - Modifiable risk factors and survival in women diagnosed with primary breast cancer: results from a prospective cohort study. PG - 366-73 AB - This study examines the impact of smoking, body mass index, alcohol consumption, hormone replacement therapy, and physical activity on all-cause mortality among 528 Danish women diagnosed with primary breast cancer. Participants were women enrolled in the Copenhagen City Heart Study. Prospective self-reported exposure information was collected from four points of follow-up in 1976-1978, 1981-1983, 1991-1994, and 2001-2003. Kaplan-Meier survival curves and multivariate Cox regression analyses were performed adjusting for age, disease stage, adjuvant treatment, menopausal status, parity, alcohol intake, smoking, physical activity, body mass index, and hormone replacement therapy. The study shows that smoking for total mortality [hazard ratio, 1.16; 95% confidence interval, 1.05-1.29] and obesity for both total mortality (1.61; 1.12-2.33) and breast cancer-specific mortality (1.82; 1.11-2.99) were significantly associated with decreased survival after breast cancer diagnosis. A moderate alcohol intake of 1-6 units/week (0.85; 0.64-1.12), 7-14 units/week (0.77; 0.56-1.08), and treatment with hormone replacement therapy (0.79; 0.59-1.05) were less than 1, but not statistically significantly associated with prolonged survival. A moderate physical activity of 2-4 h/week (1.07; 0.77-1.49) and a high physical activity of more than 4 h/week (1.00; 0.69-1.45) showed no association with survival after breast cancer diagnosis. AD - Centre for Alcohol Research, National Institute of Public Health, Copenhagen, Denmark. FAU - Hellmann, Sophie Sell AU - Hellmann SS FAU - Thygesen, Lau Caspar AU - Thygesen LC FAU - Tolstrup, Janne Schurmann AU - Tolstrup JS FAU - Gronbaek, Morten AU - Gronbaek M LA - eng PT - Journal Article PL - England TA - Eur J Cancer Prev JT - European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) JID - 9300837 SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Alcohol Drinking/mortality MH - Body Mass Index MH - Breast Neoplasms/diagnosis/*mortality MH - Cause of Death MH - Denmark/epidemiology MH - Exercise MH - Female MH - Follow-Up Studies MH - Hormone Replacement Therapy MH - Humans MH - Kaplan-Meiers Estimate MH - Middle Aged MH - Obesity/mortality MH - Prognosis MH - Prospective Studies MH - Risk Factors MH - Smoking/mortality EDAT- 2010/05/27 06:00 MHDA- 2010/11/09 06:00 CRDT- 2010/05/27 06:00 AID - 10.1097/CEJ.0b013e32833b4828 [doi] PST - ppublish SO - Eur J Cancer Prev. 2010 Sep;19(5):366-73. PMID- 20500821 OWN - NLM STAT- MEDLINE DA - 20100702 DCOM- 20101027 IS - 1471-2105 (Electronic) IS - 1471-2105 (Linking) VI - 11 DP - 2010 TI - Prediction of breast cancer prognosis using gene set statistics provides signature stability and biological context. PG - 277 AB - BACKGROUND: Different microarray studies have compiled gene lists for predicting outcomes of a range of treatments and diseases. These have produced gene lists that have little overlap, indicating that the results from any one study are unstable. It has been suggested that the underlying pathways are essentially identical, and that the expression of gene sets, rather than that of individual genes, may be more informative with respect to prognosis and understanding of the underlying biological process. RESULTS: We sought to examine the stability of prognostic signatures based on gene sets rather than individual genes. We classified breast cancer cases from five microarray studies according to the risk of metastasis, using features derived from predefined gene sets. The expression levels of genes in the sets are aggregated, using what we call a set statistic. The resulting prognostic gene sets were as predictive as the lists of individual genes, but displayed more consistent rankings via bootstrap replications within datasets, produced more stable classifiers across different datasets, and are potentially more interpretable in the biological context since they examine gene expression in the context of their neighbouring genes in the pathway. In addition, we performed this analysis in each breast cancer molecular subtype, based on ER/HER2 status. The prognostic gene sets found in each subtype were consistent with the biology based on previous analysis of individual genes. CONCLUSIONS: To date, most analyses of gene expression data have focused at the level of the individual genes. We show that a complementary approach of examining the data using predefined gene sets can reduce the noise and could provide increased insight into the underlying biological pathways. AD - Department of Computer Science and Software Engineering, The University of Melbourne, Parkville 3010, VIC, Australia. FAU - Abraham, Gad AU - Abraham G FAU - Kowalczyk, Adam AU - Kowalczyk A FAU - Loi, Sherene AU - Loi S FAU - Haviv, Izhak AU - Haviv I FAU - Zobel, Justin AU - Zobel J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100525 PL - England TA - BMC Bioinformatics JT - BMC bioinformatics JID - 100965194 RN - 0 (Tumor Markers, Biological) SB - IM MH - Breast Neoplasms/*diagnosis/*genetics MH - Female MH - Gene Expression Profiling/*methods MH - Humans MH - Prognosis MH - Tumor Markers, Biological/genetics PMC - PMC2895626 OID - NLM: PMC2895626 EDAT- 2010/05/27 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/05/27 06:00 PHST- 2010/02/08 [received] PHST- 2010/05/25 [accepted] PHST- 2010/05/25 [aheadofprint] AID - 1471-2105-11-277 [pii] AID - 10.1186/1471-2105-11-277 [doi] PST - epublish SO - BMC Bioinformatics. 2010 May 25;11:277. PMID- 20500820 OWN - NLM STAT- MEDLINE DA - 20100628 DCOM- 20101027 IS - 1471-2105 (Electronic) IS - 1471-2105 (Linking) VI - 11 DP - 2010 TI - Comparison of scores for bimodality of gene expression distributions and genome-wide evaluation of the prognostic relevance of high-scoring genes. PG - 276 AB - BACKGROUND: A major goal of the analysis of high-dimensional RNA expression data from tumor tissue is to identify prognostic signatures for discriminating patient subgroups. For this purpose genome-wide identification of bimodally expressed genes from gene array data is relevant because distinguishability of high and low expression groups is easier compared to genes with unimodal expression distributions.Recently, several methods for the identification of genes with bimodal distributions have been introduced. A straightforward approach is to cluster the expression values and score the distance between the two distributions. Other scores directly measure properties of the distribution. The kurtosis, e.g., measures divergence from a normal distribution. An alternative is the outlier-sum statistic that identifies genes with extremely high or low expression values in a subset of the samples. RESULTS: We compare and discuss scores for bimodality for expression data. For the genome-wide identification of bimodal genes we apply all scores to expression data from 194 patients with node-negative breast cancer. Further, we present the first comprehensive genome-wide evaluation of the prognostic relevance of bimodal genes. We first rank genes according to bimodality scores and define two patient subgroups based on expression values. Then we assess the prognostic significance of the top ranking bimodal genes by comparing the survival functions of the two patient subgroups. We also evaluate the global association between the bimodal shape of expression distributions and survival times with an enrichment type analysis.Various cluster-based methods lead to a significant overrepresentation of prognostic genes. A striking result is obtained with the outlier-sum statistic (p < 10-12). Many genes with heavy tails generate subgroups of patients with different prognosis. CONCLUSIONS: Genes with high bimodality scores are promising candidates for defining prognostic patient subgroups from expression data. We discuss advantages and disadvantages of the different scores for prognostic purposes. The outlier-sum statistic may be particularly valuable for the identification of genes to be included in prognostic signatures. Among the genes identified as bimodal in the breast cancer data set several have not yet previously been recognized to be prognostic and bimodally expressed in breast cancer. AD - Department of Statistics, TU Dortmund University, 44221 Dortmund, Germany. hellwig@statistik.tu-dortmund.de FAU - Hellwig, Birte AU - Hellwig B FAU - Hengstler, Jan G AU - Hengstler JG FAU - Schmidt, Marcus AU - Schmidt M FAU - Gehrmann, Mathias C AU - Gehrmann MC FAU - Schormann, Wiebke AU - Schormann W FAU - Rahnenfuhrer, Jorg AU - Rahnenfuhrer J LA - eng PT - Comparative Study PT - Evaluation Studies PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100525 PL - England TA - BMC Bioinformatics JT - BMC bioinformatics JID - 100965194 RN - 0 (Tumor Markers, Biological) SB - IM MH - Breast Neoplasms/diagnosis/genetics MH - Cluster Analysis MH - *Gene Expression MH - Gene Expression Profiling MH - *Genome MH - Humans MH - Oligonucleotide Array Sequence Analysis MH - Tumor Markers, Biological/genetics PMC - PMC2892466 OID - NLM: PMC2892466 EDAT- 2010/05/27 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/05/27 06:00 PHST- 2010/01/05 [received] PHST- 2010/05/25 [accepted] PHST- 2010/05/25 [aheadofprint] AID - 1471-2105-11-276 [pii] AID - 10.1186/1471-2105-11-276 [doi] PST - epublish SO - BMC Bioinformatics. 2010 May 25;11:276. PMID- 20497617 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - At last, a predictive and prognostic marker for radiotherapy? PG - 106 AB - Holliday junction recognition protein (HJURP) levels in breast cancer associate with both poor prognosis and an increased sensitivity to irradiation. Whilst, in part, this could be explained in relation to proliferation, it would not entirely account for the association with sensitivity to radiation. Thus, HJURP may have clinical potential as a marker of prognosis and radiation sensitivity; further validation with tissues from randomised controlled trials is needed. HJURP may represent the first in a class of proteins with roles in chromosome segregation and DNA repair that act as predictive biomarkers. FAU - Coates, Philip AU - Coates P FAU - Dewar, John AU - Dewar J FAU - Thompson, Alastair M AU - Thompson AM LA - eng PT - Comment PT - Editorial DEP - 20100511 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (DNA-Binding Proteins) RN - 0 (Holliday junction recognizing protein, human) RN - 0 (Tumor Markers, Biological) SB - IM CON - Breast Cancer Res. 2010;12(2):R18. PMID: 20211017 MH - Breast Neoplasms/diagnosis/*genetics/*radiotherapy MH - DNA Repair MH - DNA-Binding Proteins/*genetics MH - Female MH - Humans MH - Prognosis MH - Radiation Tolerance/*genetics MH - Tumor Markers, Biological/*genetics PMC - PMC2917011 OID - NLM: PMC2917011 EDAT- 2010/05/26 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/05/26 06:00 PHST- 2010/05/11 [aheadofprint] AID - bcr2567 [pii] AID - 10.1186/bcr2567 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):106. Epub 2010 May 11. PMID- 20482762 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Incorporating tumour pathology information into breast cancer risk prediction algorithms. PG - R28 AB - INTRODUCTION: Mutations in BRCA1 and BRCA2 confer high risks of breast cancer and ovarian cancer. The risk prediction algorithm BOADICEA (Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm) may be used to compute the probabilities of carrying mutations in BRCA1 and BRCA2 and help to target mutation screening. Tumours from BRCA1 and BRCA2 mutation carriers display distinctive pathological features that could be used to better discriminate between BRCA1 mutation carriers, BRCA2 mutation carriers and noncarriers. In particular, oestrogen receptor (ER)-negative status, triple-negative (TN) status, and expression of basal markers are predictive of BRCA1 mutation carrier status. METHODS: We extended BOADICEA by treating breast cancer subtypes as distinct disease end points. Age-specific expression of phenotypic markers in a series of tumours from 182 BRCA1 mutation carriers, 62 BRCA2 mutation carriers and 109 controls from the Breast Cancer Linkage Consortium, and over 300,000 tumours from the general population obtained from the Surveillance Epidemiology, and End Results database, were used to calculate age-specific and genotype-specific incidences of each disease end point. The probability that an individual carries a BRCA1 or BRCA2 mutation given their family history and tumour marker status of family members was computed in sample pedigrees. RESULTS: The cumulative risk of ER-negative breast cancer by age 70 for BRCA1 mutation carriers was estimated to be 55% and the risk of ER-positive disease was 18%. The corresponding risks for BRCA2 mutation carriers were 21% and 44% for ER-negative and ER-positive disease, respectively. The predicted BRCA1 carrier probabilities among ER-positive breast cancer cases were less than 1% at all ages. For women diagnosed with breast cancer below age 50 years, these probabilities rose to more than 5% in ER-negative breast cancer, 7% in TN disease and 24% in TN breast cancer expressing both CK5/6 and CK14 cytokeratins. Large differences in mutation probabilities were observed by combining ER status and other informative markers with family history. CONCLUSIONS: This approach combines both full pedigree and tumour subtype data to predict BRCA1/2 carrier probabilities. Prediction of BRCA1/2 carrier status, and hence selection of women for mutation screening, may be substantially improved by combining tumour pathology with family history of cancer. AD - Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Strangeways Research Laboratory, Worts Causeway, Cambridge, UK. nasim@srl.cam.ac.uk FAU - Mavaddat, Nasim AU - Mavaddat N FAU - Rebbeck, Timothy R AU - Rebbeck TR FAU - Lakhani, Sunil R AU - Lakhani SR FAU - Easton, Douglas F AU - Easton DF FAU - Antoniou, Antonis C AU - Antoniou AC LA - eng GR - Cancer Research UK/United Kingdom GR - Medical Research Council/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100518 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (BRCA1 Protein) RN - 0 (BRCA2 Protein) RN - 0 (Tumor Markers, Biological) SB - IM MH - Adult MH - Aged MH - *Algorithms MH - BRCA1 Protein/genetics MH - BRCA2 Protein/genetics MH - Breast Neoplasms/classification/*genetics/*pathology MH - Case-Control Studies MH - Female MH - *Genetic Predisposition to Disease MH - Heterozygote MH - Humans MH - Incidence MH - Middle Aged MH - Mutation/genetics MH - Ovarian Neoplasms/*genetics/*pathology MH - Pedigree MH - Prognosis MH - Tumor Markers, Biological/genetics PMC - PMC2917017 OID - NLM: PMC2917017 EDAT- 2010/05/21 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/05/21 06:00 PHST- 2010/01/22 [received] PHST- 2010/05/04 [revised] PHST- 2010/05/18 [accepted] PHST- 2010/05/18 [aheadofprint] AID - bcr2576 [pii] AID - 10.1186/bcr2576 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R28. Epub 2010 May 18. PMID- 20464479 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - CEF is superior to CMF for tumours with TOP2A aberrations: a Subpopulation Treatment Effect Pattern Plot (STEPP) analysis on Danish Breast Cancer Cooperative Group Study 89D. PG - 163-9 AB - The aim of this study was to examine TOP2A gene copy number changes as a means to identify groups of breast cancer patients with superior benefit from treatment with anthracyclines. Tumour tissue was retrospectively collected and successfully analysed for TOP2A in 773 of 980 Danish patients randomly assigned to receive intravenous CMF (cyclophosphamide, methotrexate and fluorouracil) or CEF (cyclophosphamide, epirubicin and fluorouracil) in DBCG trial 89D. Subgroup analyses on this material published by Knoop et al. (J Clin Oncol 23:7483-7490, 2005) and updated by Nielsen et al. (Acta Oncol 47:725-734, 2008) demonstrated that superiority of CEF over CMF is limited to patients with TOP2A aberrations, defined as patients whose tumours have TOP2A ratio below 0.8 or above 2.0. The Subpopulation Treatment Effect Pattern Plot (STEPP) technique was applied to these data to explore the pattern of treatment effect relative to TOP2A and to compare that pattern to the ranges previously used to define 'aberrations'. The pattern of treatment effect illustrated by the STEPP analysis confirmed that the superiority of CEF over CMF is indeed limited to patients whose tumours have high or low TOP2A ratios. The hypothesis of no treatment effect-covariate interaction was rejected (P = 0.02). Furthermore, results indicated that the interval of TOP2A ratios hitherto denoted as 'normal' could be narrower than previously assumed. A more optimal separation of TOP2A subgroups could be obtained by altering cut-points currently used to define TOP2A amplified and TOP2A deleted tumours by narrowing the TOP2A normal interval, and consequently enlarging the population with TOP2A aberrated tumours. AD - Danish Breast Cancer Cooperative Group, DBCG Secretariat, Rigshospitalet, Bldg 2501 9, Blegdamsvej, 2100 Copenhagen, Denmark. FAU - Gunnarsdottir, Katrin A AU - Gunnarsdottir KA FAU - Jensen, Maj-Britt AU - Jensen MB FAU - Zahrieh, David AU - Zahrieh D FAU - Gelber, Richard D AU - Gelber RD FAU - Knoop, Ann AU - Knoop A FAU - Bonetti, Marco AU - Bonetti M FAU - Mouridsen, Henning AU - Mouridsen H FAU - Ejlertsen, Bent AU - Ejlertsen B LA - eng GR - CA-75362/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20100513 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Antigens, Neoplasm) RN - 0 (CMF protocol) RN - 0 (DNA-Binding Proteins) RN - 15663-27-1 (Cisplatin) RN - 50-18-0 (Cyclophosphamide) RN - 51-21-8 (Fluorouracil) RN - 56420-45-2 (Epirubicin) RN - 59-05-2 (Methotrexate) RN - EC 5.99.1.- (DNA Topoisomerases, Type II, Eukaryotic) RN - EC 5.99.1.3 (DNA topoisomerase II alpha) SB - IM CIN - Breast Cancer Res Treat. 2010 Aug;123(1):171-5. PMID: 20549335 MH - Antigens, Neoplasm/*genetics MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Breast Neoplasms/*drug therapy/*genetics/mortality MH - Cisplatin MH - Cyclophosphamide/administration & dosage MH - DNA Topoisomerases, Type II, Eukaryotic/*genetics MH - DNA-Binding Proteins/*genetics MH - Data Interpretation, Statistical MH - Disease-Free Survival MH - Drug Resistance, Neoplasm/genetics MH - Epirubicin/administration & dosage MH - Female MH - Fluorouracil/administration & dosage MH - Gene Dosage MH - Humans MH - In Situ Hybridization, Fluorescence MH - Methotrexate/administration & dosage MH - *Randomized Controlled Trials as Topic MH - Treatment Outcome EDAT- 2010/05/14 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/05/14 06:00 PHST- 2009/12/30 [received] PHST- 2010/04/28 [accepted] PHST- 2010/05/13 [aheadofprint] AID - 10.1007/s10549-010-0931-y [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):163-9. Epub 2010 May 13. PMID- 20462826 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101102 IS - 1877-783x (Electronic) VI - 34 IP - 4 DP - 2010 Aug TI - Assessment of women's risk factors for breast cancer and predictors of the practice of breast examination in two rural areas near Ibadan, Nigeria. PG - 425-8 AB - OBJECTIVE: In Nigeria, breast cancer is the most common cancer among women in majority of the regions. Late presentation has also been reported for about four decades. This study assessed the women's risk factors for breast cancer and predictive factors for the practice of breast examinations. The findings will be of help in enhancing early detection of the disease and reducing mortality from the disease. METHODS: Utilizing a multi-stage sampling method, 420 women were selected at Akinyele Local government area of Ibadan. Data was collected with questionnaire. The risk factor was evaluated using the breast cancer risk assessment tool based on the Gail model. Six demographic factors, plus four covariates: knowledge of BSE/CBE, knowledge of the cause of, symptoms and signs of and treatment of breast cancer, were regressed against two dependent variables of practice of BSE and CBE using linear regression and binary logistic analyses respectively. RESULTS: Only 386 questionnaires properly filled were analyzed. The mean age of respondents was 37.3 (SD=13.1) years. They were of low educational status and were mostly traders and married. Only 190 of the women fulfilled the criteria for assessment with the Gail model. Most of the women, 180 (94.7%), had five years and 184 (96.8%) had lifetime risks lower than that of the average woman of the same age. Four significant predictors of BSE were marital status (p=0.004), educational status (p=0.018), knowledge of treatment of breast cancer (p=0.029) and knowledge of BSE/CBE (p=0.0001) while no formal education status and being a farmer were the only significant predictors of CBE. CONCLUSIONS: The findings are useful for planning interventional studies to enhance early detection in a low resource country. AD - Department of Nursing, University of Ibadan, Ibadan, Nigeria. aoluwatosin@yahoo.com FAU - Oluwatosin, O Abimbola AU - Oluwatosin OA LA - eng PT - Journal Article PT - Randomized Controlled Trial DEP - 20100512 PL - Netherlands TA - Cancer Epidemiol JT - Cancer epidemiology JID - 101508793 SB - IM MH - Adult MH - Breast Neoplasms/*diagnosis/epidemiology MH - Breast Self-Examination/*utilization MH - Female MH - *Health Knowledge, Attitudes, Practice MH - Humans MH - Mammography/*psychology MH - Middle Aged MH - Nigeria/epidemiology MH - Questionnaires MH - Risk Factors MH - Rural Population/*statistics & numerical data MH - Survival Rate MH - Women's Health MH - Young Adult EDAT- 2010/05/14 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/05/14 06:00 PHST- 2009/09/03 [received] PHST- 2010/04/04 [revised] PHST- 2010/04/09 [accepted] PHST- 2010/05/12 [aheadofprint] AID - S1877-7821(10)00067-6 [pii] AID - 10.1016/j.canep.2010.04.005 [doi] PST - ppublish SO - Cancer Epidemiol. 2010 Aug;34(4):425-8. Epub 2010 May 12. PMID- 20459744 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - Cyclophosphamide-metabolizing enzyme polymorphisms and survival outcomes after adjuvant chemotherapy for node-positive breast cancer: a retrospective cohort study. PG - R26 AB - INTRODUCTION: Cyclophosphamide-based adjuvant chemotherapy is a mainstay of treatment for women with node-positive breast cancer, but is not universally effective in preventing recurrence. Pharmacogenetic variability in drug metabolism is one possible mechanism of treatment failure. We hypothesize that functional single nucleotide polymorphisms (SNPs) in drug metabolizing enzymes (DMEs) that activate (CYPs) or metabolize (GSTs) cyclophosphamide account for some of the observed variability in disease outcomes. METHODS: We performed a retrospective cohort study of 350 women enrolled in a multicenter, randomized, adjuvant breast cancer chemotherapy trial (ECOG-2190/INT-0121). Subjects in this trial received standard-dose cyclophosphamide, doxorubicin and fluorouracil (CAF), followed by either observation or high-dose cyclophosphamide and thiotepa with stem cell rescue. We used bone marrow stem cell-derived genomic DNA from archival specimens to genotype CYP2B6, CYP2C9, CYP2D6, CYP3A4, CYP3A5, GSTM1, GSTT1, and GSTP1. Cox regression models were computed to determine associations between genotypes (individually or in combination) and disease-free survival (DFS) or overall survival (OS), adjusting for confounding clinical variables. RESULTS: In the full multivariable analysis, women with at least one CYP3A4 *1B variant allele had significantly worse DFS than those who were wild-type *1A/*1A (multivariate hazard ratio 2.79; 95% CI 1.52, 5.14). CYP2D6 genotype did not impact this association among patients with estrogen receptor (ER) -positive tumors scheduled to receive tamoxifen. CONCLUSIONS: These data support the hypothesis that genetic variability in cyclophosphamide metabolism independently impacts outcome from adjuvant chemotherapy for breast cancer. AD - Center for Cancer and Hematologic Disease, 1930 E. Route 70, Cherry Hill, NJ 08003, USA. priyagor@hotmail.com FAU - Gor, Priya P AU - Gor PP FAU - Su, H Irene AU - Su HI FAU - Gray, Robert J AU - Gray RJ FAU - Gimotty, Phyllis A AU - Gimotty PA FAU - Horn, Michelle AU - Horn M FAU - Aplenc, Richard AU - Aplenc R FAU - Vaughan, William P AU - Vaughan WP FAU - Tallman, Martin S AU - Tallman MS FAU - Rebbeck, Timothy R AU - Rebbeck TR FAU - DeMichele, Angela AU - DeMichele A LA - eng GR - K23 HD058799-03/HD/NICHD NIH HHS/United States GR - R01-CA104581/CA/NCI NIH HHS/United States GR - T32-CA-009679/CA/NCI NIH HHS/United States PT - Journal Article PT - Multicenter Study PT - Randomized Controlled Trial PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20100510 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (Tumor Markers, Biological) RN - 23214-92-8 (Doxorubicin) RN - 50-18-0 (Cyclophosphamide) RN - 51-21-8 (Fluorouracil) RN - 52-24-4 (Thiotepa) RN - EC 1.14.13.67 (CYP3A4 protein, human) RN - EC 1.14.14.1 (Cytochrome P-450 CYP3A) SB - IM MH - Adult MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Breast Neoplasms/drug therapy/*enzymology/*genetics MH - Chemotherapy, Adjuvant MH - Cohort Studies MH - Cyclophosphamide/administration & dosage MH - Cytochrome P-450 CYP3A/*genetics MH - Doxorubicin/administration & dosage MH - Female MH - Fluorouracil/administration & dosage MH - Humans MH - Lymph Nodes/enzymology/pathology MH - Lymphatic Metastasis MH - Middle Aged MH - Polymorphism, Single Nucleotide/*genetics MH - Retrospective Studies MH - Survival Rate MH - Thiotepa/administration & dosage MH - Treatment Outcome MH - Tumor Markers, Biological/*genetics PMC - PMC2917014 OID - NLM: PMC2917014 EDAT- 2010/05/13 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/05/13 06:00 PHST- 2009/09/18 [received] PHST- 2010/03/24 [revised] PHST- 2010/05/10 [accepted] PHST- 2010/05/10 [aheadofprint] AID - bcr2570 [pii] AID - 10.1186/bcr2570 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R26. Epub 2010 May 10. PMID- 20459607 OWN - NLM STAT- MEDLINE DA - 20100806 DCOM- 20101115 IS - 1465-542X (Electronic) IS - 1465-5411 (Linking) VI - 12 IP - 3 DP - 2010 TI - High-resolution genomic and expression analyses of copy number alterations in HER2-amplified breast cancer. PG - R25 AB - INTRODUCTION: HER2 gene amplification and protein overexpression (HER2+) define a clinically challenging subgroup of breast cancer with variable prognosis and response to therapy. Although gene expression profiling has identified an ERBB2 molecular subtype of breast cancer, it is clear that HER2+ tumors reside in all molecular subtypes and represent a genomically and biologically heterogeneous group, needed to be further characterized in large sample sets. METHODS: Genome-wide DNA copy number profiling, using bacterial artificial chromosome (BAC) array comparative genomic hybridization (aCGH), and global gene expression profiling were performed on 200 and 87 HER2+ tumors, respectively. Genomic Identification of Significant Targets in Cancer (GISTIC) was used to identify significant copy number alterations (CNAs) in HER2+ tumors, which were related to a set of 554 non-HER2 amplified (HER2-) breast tumors. High-resolution oligonucleotide aCGH was used to delineate the 17q12-q21 region in high detail. RESULTS : The HER2-amplicon was narrowed to an 85.92 kbp region including the TCAP, PNMT, PERLD1, HER2, C17orf37 and GRB7 genes, and higher HER2 copy numbers indicated worse prognosis. In 31% of HER2+ tumors the amplicon extended to TOP2A, defining a subgroup of HER2+ breast cancer associated with estrogen receptor-positive status and with a trend of better survival than HER2+ breast cancers with deleted (18%) or neutral TOP2A (51%). HER2+ tumors were clearly distinguished from HER2- tumors by the presence of recurrent high-level amplifications and firestorm patterns on chromosome 17q. While there was no significant difference between HER2+ and HER2- tumors regarding the incidence of other recurrent high-level amplifications, differences in the co-amplification pattern were observed, as shown by the almost mutually exclusive occurrence of 8p12, 11q13 and 20q13 amplification in HER2+ tumors. GISTIC analysis identified 117 significant CNAs across all autosomes. Supervised analyses revealed: (1) significant CNAs separating HER2+ tumors stratified by clinical variables, and (2) CNAs separating HER2+ from HER2- tumors. CONCLUSIONS: We have performed a comprehensive survey of CNAs in HER2+ breast tumors, pinpointing significant genomic alterations including both known and potentially novel therapeutic targets. Our analysis sheds further light on the genomically complex and heterogeneous nature of HER2+ tumors in relation to other subgroups of breast cancer. AD - Department of Oncology, Clinical Sciences, Lund University, Barngatan 2B, Lund, Sweden. johan.staaf@med.lu.se FAU - Staaf, Johan AU - Staaf J FAU - Jonsson, Goran AU - Jonsson G FAU - Ringner, Markus AU - Ringner M FAU - Vallon-Christersson, Johan AU - Vallon-Christersson J FAU - Grabau, Dorthe AU - Grabau D FAU - Arason, Adalgeir AU - Arason A FAU - Gunnarsson, Haukur AU - Gunnarsson H FAU - Agnarsson, Bjarni A AU - Agnarsson BA FAU - Malmstrom, Per-Olof AU - Malmstrom PO FAU - Johannsson, Oskar Th AU - Johannsson OT FAU - Loman, Niklas AU - Loman N FAU - Barkardottir, Rosa B AU - Barkardottir RB FAU - Borg, Ake AU - Borg A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100506 PL - England TA - Breast Cancer Res JT - Breast cancer research : BCR JID - 100927353 RN - 0 (Tumor Markers, Biological) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CIN - Breast Cancer Res. 2010;12(3):107. PMID: 20519027 MH - Adult MH - Aged MH - Aged, 80 and over MH - Breast Neoplasms/*genetics/pathology MH - Chromosomes, Artificial, Bacterial MH - Chromosomes, Human, Pair 17/genetics MH - Female MH - *Gene Amplification MH - *Gene Dosage MH - *Gene Expression Profiling MH - *Genome, Human MH - Humans MH - Middle Aged MH - Oligonucleotide Array Sequence Analysis MH - Prognosis MH - Receptor, erbB-2/*genetics MH - Survival Rate MH - Tumor Markers, Biological/*genetics PMC - PMC2917012 OID - NLM: PMC2917012 EDAT- 2010/05/13 06:00 MHDA- 2010/11/16 06:00 CRDT- 2010/05/13 06:00 PHST- 2009/11/17 [received] PHST- 2010/03/05 [revised] PHST- 2010/05/06 [accepted] PHST- 2010/05/06 [aheadofprint] AID - bcr2568 [pii] AID - 10.1186/bcr2568 [doi] PST - ppublish SO - Breast Cancer Res. 2010;12(3):R25. Epub 2010 May 6. PMID- 20451485 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101102 IS - 1877-783x (Electronic) VI - 34 IP - 4 DP - 2010 Aug TI - Identification of novel large genomic rearrangements at the BRCA1 locus in Malaysian women with breast cancer. PG - 442-7 AB - BACKGROUND: The incidence of breast cancer has been on the rise in Malaysia. It is suggested that a subset of breast cancer cases were associated with germline mutation in breast cancer susceptibility (BRCA) genes. Most of the BRCA mutations reported in Malaysia were point mutations, small deletions and insertions. Here we report the first study of BRCA large genomic rearrangements (LGRs) in Malaysia. We aimed to detect the presence of LGRs in the BRCA genes of Malaysian patients with breast cancer. METHODS: Multiplex ligation-dependent probe amplification (MLPA) for BRCA LGRs was carried out on 100 patients (60 were high-risk breast cancer patients previously tested negative/positive for BRCA1 and BRCA2 mutations, and 40 were sporadic breast cancer patients), recruited from three major referral centres, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Hospital Kuala Lumpur (HKL) and Hospital Putrajaya (HPJ). Results: Two novel BRCA1 rearrangements were detected in patients with sporadic breast cancer; both results were confirmed by quantitative PCR. No LGRs were found in patients with high-risk breast cancer. The two large genomic rearrangements detected were genomic amplifications of exon 3 and exon 10. No BRCA2 genomic rearrangement was found in both high-risk and sporadic breast cancer patients. CONCLUSION: These results will be helpful to understand the mutation spectrum of BRCA1 and BRCA2 genes in Malaysian patients with breast cancer. Further studies involving larger samples are required to establish a genetic screening strategy for both high-risk and sporadic breast cancer patients. AD - Department of Pathology, Universiti Kebangsaan Malaysia Medical Centre, Cheras, Kuala Lumpur, Malaysia. sharifah@ppukm.ukm.my FAU - Sharifah, Noor Akmal AU - Sharifah NA FAU - Nurismah, Md Isa AU - Nurismah MI FAU - Lee, Han Chung AU - Lee HC FAU - Aisyah, Aziz Nur AU - Aisyah AN FAU - Clarence-Ko, Ching Huat AU - Clarence-Ko CH FAU - Naqiyah, Ismail AU - Naqiyah I FAU - Rohaizak, Mohamad AU - Rohaizak M FAU - Fuad, Ismail AU - Fuad I FAU - A Jamal, A Rahman AU - A Jamal AR FAU - Zarina, Abdul Latiff AU - Zarina AL FAU - Nor Aina, Emran AU - Nor Aina E FAU - Normayah, Kitan AU - Normayah K FAU - Nor Hisham, Abdullah AU - Nor Hisham A LA - eng PT - Comparative Study PT - Journal Article PT - Multicenter Study PT - Research Support, Non-U.S. Gov't DEP - 20100506 PL - Netherlands TA - Cancer Epidemiol JT - Cancer epidemiology JID - 101508793 RN - 0 (BRCA1 Protein) RN - 0 (BRCA2 Protein) RN - 0 (DNA, Neoplasm) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - BRCA1 Protein/*genetics MH - BRCA2 Protein/genetics MH - Breast Neoplasms/*genetics/pathology MH - DNA, Neoplasm/genetics MH - Female MH - *Gene Rearrangement MH - *Genetic Testing MH - *Genome, Human MH - Germ-Line Mutation/genetics MH - Humans MH - Malaysia MH - Male MH - Middle Aged MH - Polymerase Chain Reaction MH - Survival Rate EDAT- 2010/05/11 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/05/11 06:00 PHST- 2009/11/05 [received] PHST- 2010/03/29 [revised] PHST- 2010/04/12 [accepted] PHST- 2010/05/06 [aheadofprint] AID - S1877-7821(10)00072-X [pii] AID - 10.1016/j.canep.2010.04.010 [doi] PST - ppublish SO - Cancer Epidemiol. 2010 Aug;34(4):442-7. Epub 2010 May 6. PMID- 20451484 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101102 IS - 1877-783x (Electronic) VI - 34 IP - 4 DP - 2010 Aug TI - Does consanguinity lead to decreased incidence of breast cancer? PG - 413-8 AB - BACKGROUND: In the Middle East region, consanguinity remains to be a central feature where it has shown an increasing trend. Breast cancer is an extremely complex disease, characterized by a progressive multistep process caused by interactions of both environmental and genetic factors. AIM: The aim of this study was to examine the possible effect of consanguinity on the risk of breast cancer in a population with a high rate of consanguinity and find the associated risk-modifying factors. SUBJECTS AND METHODS: The study included 167 Qatari and other Arab expatriates women with breast cancer and 341 age and ethnicity matched control women. A questionnaire that included the socio-demographic information, type of consanguinity, medical history, life style habits, dietary intake and tumor grade was designed to collect, the information of cases and controls. A total number of 214 breast cancer patients were approached and 167 cases completed the questionnaires with a response rate of 78%. Of the 417 healthy women who agreed to participate in this study, 341 responded to the questionnaire (81.8%). RESULTS: The study revealed that the rate of parental consanguinity was lower in breast cancer patients (24%) than in controls (32.3%) (p=0.062). Female controls were slightly younger (46.5+/-11.9) than breast cancer patients (48.4+/-10.7). Breast cancer incidence was significantly higher in Qatari women (34.1%) compared to other Arab women (65.9%) (p=0.034). A significant difference was noted only in occupation of the studied women between cases and controls (p<0.001). Overweight (46.7%) and obesity (32.9%) were significantly higher in female breast cancer patients compared to controls (p=0.028). Overall, the mean coefficient of consanguinity was lower in breast cancer patients (0.014) than in controls (0.018) (p=0.0125). Family history of breast cancer was significantly more often in breast cancer patients (14.4%) than in controls (6.2%) (p=0.002). However, the family history of breast cancer was more often positive in cases of non-consanguineous parents (15.7%) than cases of consanguineous parents (10.0%). CONCLUSION: The present study revealed the lack of association between of breast cancer and the parental consanguinity in Arab women residing in Qatar. The family history of breast cancer and the body mass index (BMI) are highly associated with breast cancer. AD - Dept. of Medical Statistics & Epidemiology, Hamad Medical Corporation, Qatar. abener@hmc.org.qa FAU - Bener, Abdulbari AU - Bener A FAU - Ayoubi, Hanadi Rafii El AU - Ayoubi HR FAU - Ali, Awab Ibrahim AU - Ali AI FAU - Al-Kubaisi, Aisha AU - Al-Kubaisi A FAU - Al-Sulaiti, Haya AU - Al-Sulaiti H LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100506 PL - Netherlands TA - Cancer Epidemiol JT - Cancer epidemiology JID - 101508793 SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Body Mass Index MH - Breast Neoplasms/*epidemiology/genetics MH - Case-Control Studies MH - *Consanguinity MH - Female MH - Humans MH - Incidence MH - Life Style MH - Middle Aged MH - Prospective Studies MH - Qatar/epidemiology MH - Questionnaires MH - Risk Factors MH - Survival Rate MH - Young Adult EDAT- 2010/05/11 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/05/11 06:00 PHST- 2009/08/03 [received] PHST- 2010/02/25 [revised] PHST- 2010/04/09 [accepted] PHST- 2010/05/06 [aheadofprint] AID - S1877-7821(10)00066-4 [pii] AID - 10.1016/j.canep.2010.04.004 [doi] PST - ppublish SO - Cancer Epidemiol. 2010 Aug;34(4):413-8. Epub 2010 May 6. PMID- 20441774 OWN - NLM STAT- MEDLINE DA - 20100614 DCOM- 20101103 IS - 1873-2933 (Electronic) IS - 0009-9120 (Linking) VI - 43 IP - 10-11 DP - 2010 Jul TI - Clinical evaluation of developed PCR-based method with hydrolysis probes for TOP2A copy number evaluation in breast cancer samples. PG - 891-8 AB - OBJECTIVES: The objective of this study was to develop a new real time PCR-based method for quantitative detection of topoisomerase II alpha (TOP2A) aberrations and to evaluate its clinical utility in breast cancer. DESIGN AND METHODS: The method applied dually labelled hydrolysis probes and Pfaffl quantification method. The study group consisted of 83 consecutive breast cancer patients. RESULTS: In the examined tumour samples median TOP2A gene dosage was 1.08 (range 0.34-7.55). TOP2A amplifications were found in 12 tumours (14.5%), no deletion was detected. Statistically significant positive correlation of TOP2A gene dosage with nodal status, tumour grade, and HER2 protein status was found. TOP2A status also correlated with disease free survival. CONCLUSIONS: The newly developed real time PCR assay showed to be fast and easy to perform. Determined by the method TOP2A gene dosage was shown to be a potent prognostic factor in breast cancer. CI - Copyright 2010 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. AD - Department of Medical Biotechnology, Intercollegiate Faculty of Biotechnology, University of Gdansk and Medical University of Gdansk, Gdansk, Poland. azaczek@gumed.edu.pl FAU - Zaczek, Anna AU - Zaczek A FAU - Markiewicz, Aleksandra AU - Markiewicz A FAU - Jaskiewicz, Janusz AU - Jaskiewicz J FAU - Pienkowski, Tadeusz AU - Pienkowski T FAU - Rhone, Piotr AU - Rhone P FAU - Jassem, Jacek AU - Jassem J FAU - Welnicka-Jaskiewicz, Marzena AU - Welnicka-Jaskiewicz M LA - eng PT - Evaluation Studies PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100502 PL - United States TA - Clin Biochem JT - Clinical biochemistry JID - 0133660 RN - 0 (Antigens, Neoplasm) RN - 0 (DNA-Binding Proteins) RN - 0 (Oligonucleotide Probes) RN - EC 5.99.1.- (DNA Topoisomerases, Type II, Eukaryotic) RN - EC 5.99.1.3 (DNA topoisomerase II alpha) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Antigens, Neoplasm/*genetics MH - Breast Neoplasms/*genetics MH - DNA Topoisomerases, Type II, Eukaryotic/*genetics MH - DNA-Binding Proteins/*genetics MH - Female MH - Gene Dosage/*genetics MH - Humans MH - Hydrolysis MH - Middle Aged MH - Oligonucleotide Probes/*genetics MH - Reverse Transcriptase Polymerase Chain Reaction/*methods EDAT- 2010/05/06 06:00 MHDA- 2010/11/04 06:00 CRDT- 2010/05/06 06:00 PHST- 2010/01/28 [received] PHST- 2010/03/31 [revised] PHST- 2010/04/17 [accepted] PHST- 2010/05/02 [aheadofprint] AID - S0009-9120(10)00193-1 [pii] AID - 10.1016/j.clinbiochem.2010.04.060 [doi] PST - ppublish SO - Clin Biochem. 2010 Jul;43(10-11):891-8. Epub 2010 May 2. PMID- 20434974 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101102 IS - 1877-783x (Electronic) VI - 34 IP - 4 DP - 2010 Aug TI - Estimating key parameters in periodic breast cancer screening-application to the Canadian National Breast Screening Study data. PG - 429-33 AB - PROBLEM STATEMENT: Breast cancer screening in women of younger age has been controversial. The screening sensitivities, transition probabilities and sojourn time distributions are estimated for females aged 40-49 years and 50-59 years separately, using the Canadian National Breast Screening Study (CNBSS) data. The purpose is to estimate the lead time distribution and the probability of not detecting the cancer early. APPROACH: Within the 40-49-year-old and 50-59-year-old cohorts separately, the age-independent statistical model was applied. Bayesian estimators along with 95% highest probability density (HPD) credible intervals (CI) were calculated. Bayesian hypothesis testing was used to compare the parameter estimates of the two cohorts. The lead time density was also estimated for both the 40-49 and 50-59-year-old cohorts. RESULTS: The screening sensitivity, transition probability of the disease, and mean sojourn time were all found to increase with age. For the 40-49-year-old and 50-59-year-old cohorts, the posterior mean sensitivities were 0.70 (95% HPD-CI: 0.46, 0.93) and 0.77 (0.61, 0.93), respectively. The posterior mean transition probabilities were 0.0023 (0.0018, 0.0027) and 0.0031 (0.0024, 0.0038), while the posterior mean sojourn times were 2.55 (1.56, 4.26) years and 3.15 (2.12, 4.96) years. Bayes factors for the ratio of posterior probabilities that the respective parameter was larger vs. smaller in the 50-59-year-old cohort were estimated to be 2.09, 40.8 and 3.0 for the sensitivity, transition probability, and mean sojourn time, respectively. All three Bayes factors were larger than two, indicating greater than 2:1 odds in favor of the hypothesis that each of these parameters was greater in the 50-59-year-old cohort. The estimated mean lead times were 0.83 years and 0.96 years if the two cohorts were screened annually. CONCLUSIONS: The increase in sensitivity corresponds to an increase in the mean sojourn time. Breast cancer in younger women is more difficult to detect by screening tests and is more aggressive than breast cancer in older women. Women aged 50-59 tend to benefit more from screening compared with women aged 40-49. AD - Department of Bioinformatics and Biostatistics, School of Public Health and Informatics Science, University of Louisville, Louisville, KY 40202, USA. FAU - Chen, Yinlu AU - Chen Y FAU - Brock, Guy AU - Brock G FAU - Wu, Dongfeng AU - Wu D LA - eng GR - P20-RR/DE177702/DE/NIDCR NIH HHS/United States GR - P20RR16481/RR/NCRR NIH HHS/United States GR - P30-ES014443/ES/NIEHS NIH HHS/United States GR - R01-HD053509/HD/NICHD NIH HHS/United States GR - R01DE018215/DE/NIDCR NIH HHS/United States GR - R03CA115012/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - Netherlands TA - Cancer Epidemiol JT - Cancer epidemiology JID - 101508793 SB - IM MH - Adult MH - Bayes Theorem MH - Breast Neoplasms/epidemiology/*prevention & control MH - Canada/epidemiology MH - *Early Detection of Cancer MH - Female MH - Humans MH - *Mammography MH - *Mass Screening MH - Middle Aged MH - *Models, Statistical MH - Risk Factors MH - Survival Rate PMC - PMC2910214 MID - NIHMS196391 OID - NLM: NIHMS196391 [Available on 08/01/11] OID - NLM: PMC2910214 [Available on 08/01/11] EDAT- 2010/05/04 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/05/04 06:00 PMCR- 2011/08/01 PHST- 2010/01/07 [received] PHST- 2010/03/11 [revised] PHST- 2010/04/04 [accepted] AID - S1877-7821(10)00063-9 [pii] AID - 10.1016/j.canep.2010.04.001 [doi] PST - ppublish SO - Cancer Epidemiol. 2010 Aug;34(4):429-33. PMID- 20407466 OWN - NLM STAT- MEDLINE DA - 20100728 DCOM- 20101101 IS - 1476-5438 (Electronic) IS - 1018-4813 (Linking) VI - 18 IP - 8 DP - 2010 Aug TI - Risk of breast and prostate cancer is not associated with increased homozygosity in outbred populations. PG - 909-14 AB - Regions of restricted genetic heterogeneity due to identity by descent (autozygosity) are known to confer susceptibility to a number of diseases. Regions of germline homozygosity (ROHs) of 1-2 Mb, the result of autozygosity, are detectable at high frequency in outbred populations. Recent studies have reported that ROHs, possibly through exposing recessive disease-causing alleles or alternative mechanisms, are associated with an increased cancer risk. To examine whether homozygosity is associated with breast or prostate cancer risk, we analysed 500K single-nucleotide polymorphism data from two genome-wide association studies conducted by the Cancer Genetics Markers of Susceptibility initiatives (http://cgems.cancer.gov/). Six common ROHs were associated with breast cancer risk and four with prostate cancer (P<0.01). Intriguingly, one of the breast cancer ROHs maps to 6q22.31-6q22.3, a region that has been previously shown to confer breast cancer risk. Although none of the ROHs remained significantly associated with cancer risk after adjustment for multiple testing, a number of ROHs merit further interrogation. However, our findings provide no strong evidence that levels of measured homozygosity, whatever their aetiology (autozygosity, uniparental isodisomy or hemizygosity), confer an increased risk of developing breast or prostate cancer in predominantly outbred populations. AD - Section of Cancer Genetics, Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey, UK. FAU - Enciso-Mora, Victor AU - Enciso-Mora V FAU - Hosking, Fay J AU - Hosking FJ FAU - Houlston, Richard S AU - Houlston RS LA - eng GR - C1298/A8362/Cancer Research UK/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100421 PL - England TA - Eur J Hum Genet JT - European journal of human genetics : EJHG JID - 9302235 RN - 0 (Genetic Markers) SB - IM MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - Female MH - Genetic Markers MH - *Genetic Predisposition to Disease MH - Genetic Variation MH - Genome-Wide Association Study MH - *Homozygote MH - Humans MH - Male MH - Polymorphism, Single Nucleotide MH - Prostatic Neoplasms/epidemiology/*genetics MH - Risk EDAT- 2010/04/22 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/04/22 06:00 PHST- 2010/04/21 [aheadofprint] AID - ejhg201053 [pii] AID - 10.1038/ejhg.2010.53 [doi] PST - ppublish SO - Eur J Hum Genet. 2010 Aug;18(8):909-14. Epub 2010 Apr 21. PMID- 20385443 OWN - NLM STAT- MEDLINE DA - 20101018 DCOM- 20101102 IS - 1532-1967 (Electronic) IS - 0305-7372 (Linking) VI - 36 IP - 7 DP - 2010 Nov TI - Targeting DNA repair in breast cancer: a clinical and translational update. PG - 557-65 AB - DNA-repair mechanisms play an important role in the maintenance of DNA integrity and protection against DNA damage. Deregulation of these mechanisms is associated with the development of cancer as is seen in breast tumours with mutations in genes like BRCA1 and BRCA2. Recent biologic findings suggest that in tumours in which one DNA repair pathway is deficient, concomitant inhibition of other repair pathways could have potential synergistic activity. Pharmacological inhibition of Poly (ADP-ribose) polymerase (PARP), a key element of the base excision repair pathway, can have synthetic lethality in tumours with deficient homologous recombination. These findings have paved the way for the clinical development of PARP inhibitors in breast tumours especially in patients with germline mutations in the BRCA1 and/or BRCA2, a population known to have deficient homologous recombination. Patients with sporadic breast cancer, especially those with a basal-like profile may also develop cancer which is deficient in DNA repair and may be susceptible to PARP inhibition. In this review we will update the clinical and biological data underlying the development of drugs targeting DNA repair with a focus on breast cancer. CI - Copyright (c) 2010 Elsevier Ltd. All rights reserved. AD - Medical Oncology Department, Princess Margaret Hospital, 610 University Avenue, Toronto, Canada. FAU - Amir, Eitan AU - Amir E FAU - Seruga, Bostjan AU - Seruga B FAU - Serrano, Rosario AU - Serrano R FAU - Ocana, Alberto AU - Ocana A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20100410 PL - Netherlands TA - Cancer Treat Rev JT - Cancer treatment reviews JID - 7502030 RN - EC 2.4.2.30 (PARP1 protein, human) RN - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases) RN - EC 3.1.3.48 (PTEN protein, human) RN - EC 3.1.3.67 (PTEN Phosphohydrolase) SB - IM MH - Breast Neoplasms/*drug therapy/etiology/*genetics MH - DNA Repair/*drug effects MH - Drug Resistance, Neoplasm MH - Female MH - Genes, BRCA1 MH - Genes, BRCA2 MH - Humans MH - PTEN Phosphohydrolase/physiology MH - Poly(ADP-ribose) Polymerases/antagonists & inhibitors EDAT- 2010/04/14 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/04/14 06:00 PHST- 2010/01/13 [received] PHST- 2010/03/12 [revised] PHST- 2010/03/16 [accepted] PHST- 2010/04/10 [aheadofprint] AID - S0305-7372(10)00058-7 [pii] AID - 10.1016/j.ctrv.2010.03.006 [doi] PST - ppublish SO - Cancer Treat Rev. 2010 Nov;36(7):557-65. Epub 2010 Apr 10. PMID- 20376556 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Effect of BRCA1/2 mutation on short-term and long-term breast cancer survival: a systematic review and meta-analysis. PG - 11-25 AB - Reports of BRCA genetic mutations and risk of death or recurrence are inconsistent. This study aimed to compare overall and disease-free breast cancer survival rates between BRCA1/2 mutation carriers and non-carriers for short-term and long-term outcomes separately. We searched the PUBMED and EMBASE databases and retrieved 452 articles using keywords that included breast cancer, BRCA mutation, and survival. Seventeen articles were selected for systematic review and among them 11 were included in our meta-analysis. We used the random-effects model to calculate the summary hazard ratio and corresponding 95% confidence interval. BRCA1 mutation carriers had significantly lower short-term and long-term overall survival rates (OSR) relative to non-carriers (HR = 1.92 [95% CI = 1.45-2.53]; 1.33 [1.12-1.58], respectively), while both short-term and long-term OSR of BRCA2 carriers did not differ from non-carriers (HR = 1.30 [95% CI = 0.95-1.76]; 1.12 [95% CI = 0.86-1.45], respectively). For short-term progression-free survival rate (PFSR), BRCA1 mutation carriers had a significantly lower rate than non-carriers (HR = 1.54 [95% CI = 1.12-2.12]), while BRCA2 mutation carriers had a similar PFSR (HR = 1.23 [95% CI = 0.96-1.58]). For long-term PFSRs, we found no significant results. Our results suggest that BRCA1 mutation decreases short-term and long-term OSRs and short-term PFSR, however, BRCA2 mutation does not affect either short-term or long-term survival rate, which is attributed to the different carcinogenic pathways for BRCA1 and BRCA2. AD - Cancer Early Detection Branch, National Cancer Control Institute, National Cancer Center, Goyang-si, Gyeonggi-do 410-769, Korea. FAU - Lee, Eun-Ha AU - Lee EH FAU - Park, Sue K AU - Park SK FAU - Park, Boyoung AU - Park B FAU - Kim, Sung-Won AU - Kim SW FAU - Lee, Min Hyuk AU - Lee MH FAU - Ahn, Sei Hyun AU - Ahn SH FAU - Son, Byung Ho AU - Son BH FAU - Yoo, Keun-Young AU - Yoo KY FAU - Kang, Daehee AU - Kang D CN - KOHBRA Research Group CN - Korean Breast Cancer Society LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20100408 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 SB - IM MH - Breast Neoplasms/*genetics/mortality/therapy MH - Disease-Free Survival MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Humans MH - *Mutation MH - Proportional Hazards Models MH - Survival Rate MH - Time Factors IR - Son BH FIR - Son, Byung Ho IR - Moon BI FIR - Moon, Byung-In IR - Yom CK FIR - Yom, Cha Kyong IR - Lee CH FIR - Lee, Chang Hyun IR - Yoon D FIR - Yoon, Dae sung IR - Noh DY FIR - Noh, Dong-Young IR - Choi DH FIR - Choi, Doo Ho IR - Chang ED FIR - Chang, Eun-deok IR - Lee HK FIR - Lee, Hae Kyung IR - Lee H FIR - Lee, Hyde IR - Kim HA FIR - Kim, Hyun-Ah IR - Youn HJ FIR - Youn, Hyun Jo IR - Lee IK FIR - Lee, Il-kyun IR - Lee JY FIR - Lee, Jee-yeon IR - Lee JE FIR - Lee, Jeong Eon IR - Ryu JW FIR - Ryu, Jin Woo IR - Jeong J FIR - Jeong, Joon IR - Yang JH FIR - Yang, Jung-Hyun IR - Hwang KT FIR - Hwang, Ki-Tae IR - Kim KS FIR - Kim, Ku Sang IR - Hur MH FIR - Hur, Min Hee IR - Lee MH FIR - Lee, Min Hyuk IR - Chang MC FIR - Chang, Myung-chul IR - Kim LS FIR - Kim, Lee Su IR - Ahn SH FIR - Ahn, Sei Hyun IR - Kim SJ FIR - Kim, Sei Joong IR - Nam SJ FIR - Nam, Seok-Jin IR - Ko SS FIR - Ko, Seung Sang IR - Han S FIR - Han, SongYee IR - Park SK FIR - Park, Sue K IR - Jung SH FIR - Jung, Sung Hoo IR - Kim SW FIR - Kim, Sung-Won IR - Kim SY FIR - Kim, Sung Yong IR - Han W FIR - Han, Wonshik IR - Noh WC FIR - Noh, Woo-Chul IR - Park YL FIR - Park, Yong Lai IR - Jung Y FIR - Jung, Yongsik IR - Suh YJ FIR - Suh, Young Jin IR - Bae YT FIR - Bae, Young Tae IR - Cho YU FIR - Cho, Young Up EDAT- 2010/04/09 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/04/09 06:00 PHST- 2009/10/01 [received] PHST- 2010/03/17 [accepted] PHST- 2010/04/08 [aheadofprint] AID - 10.1007/s10549-010-0859-2 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):11-25. Epub 2010 Apr 8. PMID- 20371218 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101102 IS - 1877-783x (Electronic) VI - 34 IP - 4 DP - 2010 Aug TI - TYMS, MTHFR, p53 and MDR1 gene polymorphisms in breast cancer patients treated with adjuvant therapy. PG - 490-3 AB - PURPOSE: The distribution of TSER (TYMS), C677T (MTHFR), Arg72Pro (p53) and C3435T (MDR1) gene polymorphisms was investigated in 80 consecutive breast cancer patients treated with adjuvant chemotherapy. RESULTS: Observed allelic frequencies were: TSER, (2) 0.55 and (3) 0.45; MTHFR C677T, (C) 0.65 and (T) 0.35; p53 Arg72Pro, (Arg) 0.76 and (Pro) 0.24; MDR1 C3435T, (C) 0.51 and (T) 0.49. MTHFR C677T was found to be a strong predictor of the presence of multifocal tumour (odds ratio, 4.1; 95% CI, 1.1-15.7; P=0.035). CONCLUSION: Our data indicate that breast cancer patients with the C/C variant may present multifocal tumour most frequently. AD - Clinical Science Department, Universidad de Las Palmas de Gran Canaria, Spain. lhenriquez@dcc.ulpgc.es FAU - Henriquez-Hernandez, Luis Alberto AU - Henriquez-Hernandez LA FAU - Perez, Leandro Fernandez AU - Perez LF FAU - Hernandez, Ana Gonzalez AU - Hernandez AG FAU - de Leon, Antonio Cabrera AU - de Leon AC FAU - Diaz-Chico, Bonifacio AU - Diaz-Chico B FAU - Rosales, A Murias AU - Rosales AM LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100403 PL - Netherlands TA - Cancer Epidemiol JT - Cancer epidemiology JID - 101508793 RN - 0 (ABCB1 protein, human) RN - 0 (P-Glycoprotein) RN - 0 (TP53 protein, human) RN - 0 (Tumor Suppressor Protein p53) RN - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2)) RN - EC 2.1.1.45 (Thymidylate Synthase) SB - IM MH - Adult MH - Aged MH - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use MH - Breast Neoplasms/drug therapy/*genetics/pathology MH - Carcinoma, Ductal, Breast/drug therapy/genetics/pathology MH - Carcinoma, Lobular/drug therapy/genetics/pathology MH - Chemotherapy, Adjuvant MH - Female MH - Genotype MH - Humans MH - Methylenetetrahydrofolate Reductase (NADPH2)/*genetics MH - Middle Aged MH - P-Glycoprotein/*genetics MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Thymidylate Synthase/*genetics MH - Tumor Suppressor Protein p53/*genetics EDAT- 2010/04/08 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/04/08 06:00 PHST- 2009/11/09 [received] PHST- 2010/02/25 [revised] PHST- 2010/03/08 [accepted] PHST- 2010/04/03 [aheadofprint] AID - S1877-7821(10)00037-8 [pii] AID - 10.1016/j.canep.2010.03.004 [doi] PST - ppublish SO - Cancer Epidemiol. 2010 Aug;34(4):490-3. Epub 2010 Apr 3. PMID- 20371181 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101105 IS - 1532-3080 (Electronic) IS - 0960-9776 (Linking) VI - 19 IP - 4 DP - 2010 Aug TI - Mammographic screening for breast cancer: An invited review of the benefits and costs. PG - 268-72 AB - Mammographic screening is a proven method for reducing breast cancer mortality for women 40 years of age and older, but the best method for implementation of mammographic screening, particularly in the age group 40-49, remains controversial. The author, in an invited review, summarizes the data and offers guidance based on the best information available for women at risk for breast cancer, and their care providers, with particular emphasis on costs and benefits. CI - 2010 Elsevier Ltd. All rights reserved. AD - Bay Area Breast Surgeons, Inc., Oakland, CA 94609, USA. jgreif@babsurgeons.com FAU - Greif, Jon M AU - Greif JM LA - eng PT - Journal Article PT - Review DEP - 20100403 PL - Netherlands TA - Breast JT - Breast (Edinburgh, Scotland) JID - 9213011 SB - IM MH - Breast Neoplasms/*diagnosis/*economics/prevention & control MH - Cost-Benefit Analysis MH - Female MH - Humans MH - Mammography/*economics/statistics & numerical data MH - Mass Screening/*economics/statistics & numerical data MH - Physical Examination/economics MH - Primary Prevention/*economics/statistics & numerical data MH - Risk Assessment/*economics/methods MH - Risk Factors MH - United States/epidemiology MH - Women's Health/economics MH - Women's Health Services/economics EDAT- 2010/04/08 06:00 MHDA- 2010/11/06 06:00 CRDT- 2010/04/08 06:00 PHST- 2010/04/03 [aheadofprint] AID - S0960-9776(10)00071-8 [pii] AID - 10.1016/j.breast.2010.03.017 [doi] PST - ppublish SO - Breast. 2010 Aug;19(4):268-72. Epub 2010 Apr 3. PMID- 20361252 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Bevacizumab and osteonecrosis of the jaw: incidence and association with bisphosphonate therapy in three large prospective trials in advanced breast cancer. PG - 181-8 AB - Long-term bisphosphonate therapy is associated with increased risk of osteonecrosis of the jaw (ONJ). In a retrospective analysis, a 16% ONJ incidence was reported in patients receiving bisphosphonates with anti-angiogenic therapy (bevacizumab or sunitinib) for bone metastases from breast, colon, or renal cell cancers. To assess ONJ incidence with bevacizumab, we analysed data from 3,560 patients receiving bevacizumab-containing therapy for locally recurrent or metastatic breast cancer (LR/MBC) in two double-blind, randomised trials (AVADO and RIBBON-1) and a large, non-randomised safety study (ATHENA). The overall incidence of ONJ with bevacizumab was 0.3% in the blinded phase of the two randomised trials and 0.4% in the single-arm study. There was a trend towards increased ONJ incidence in patients who received bisphosphonate therapy versus those with no bisphosphonate exposure (0.9 vs. 0.2%, respectively, in the pooled analysis of the randomised trials; 2.4 vs. 0%, respectively, in ATHENA). In conclusion, this is the largest analysis of ONJ in patients receiving bevacizumab for LR/MBC. The 0.3-0.4% incidence is considerably lower than previously suggested with anti-angiogenic therapy in a small retrospective analysis. The risk of ONJ appeared to be increased in patients exposed to bisphosphonates, a pattern consistent with observations before the introduction of anti-angiogenic therapy to breast cancer management. The 0.9-2.4% incidence seen in bisphosphonate-exposed patients receiving bevacizumab is within the 1-6% range reported for bisphosphonates alone. Good oral hygiene, dental examination, and avoidance of invasive dental procedures remain important in patients receiving bisphosphonates, irrespective of bevacizumab administration. AD - Department of Oncology, Hematology and Respiratory Diseases, University of Modena and Reggio Emilia, University Hospital, Via del Pozzo 71, 41100 Modena, Italy. guarneri.valentina@unimore.it FAU - Guarneri, Valentina AU - Guarneri V FAU - Miles, David AU - Miles D FAU - Robert, Nicholas AU - Robert N FAU - Dieras, Veronique AU - Dieras V FAU - Glaspy, John AU - Glaspy J FAU - Smith, Ian AU - Smith I FAU - Thomssen, Christoph AU - Thomssen C FAU - Biganzoli, Laura AU - Biganzoli L FAU - Taran, Tanya AU - Taran T FAU - Conte, PierFranco AU - Conte P LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100402 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Angiogenesis Inhibitors) RN - 0 (Antibodies, Monoclonal) RN - 0 (Antineoplastic Agents) RN - 0 (Diphosphonates) RN - 0 (Taxoids) RN - 0 (bevacizumab) RN - 114977-28-5 (docetaxel) RN - 33069-62-4 (Paclitaxel) RN - 71486-22-1 (vinorelbine) RN - 865-21-4 (Vinblastine) SB - IM CIN - Breast Cancer Res Treat. 2010 Jul;122(1):189-91. PMID: 20464477 MH - Aged MH - Angiogenesis Inhibitors/administration & dosage/*adverse effects/therapeutic use MH - Antibodies, Monoclonal/administration & dosage/*adverse effects/therapeutic use MH - Antineoplastic Agents/*adverse effects/therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/therapeutic use MH - Breast Neoplasms/complications/*drug therapy/genetics/pathology MH - Diphosphonates/*adverse effects MH - Double-Blind Method MH - Drug Synergism MH - Female MH - Genes, erbB-2 MH - Humans MH - Incidence MH - Jaw Diseases/*chemically induced/epidemiology/prevention & control MH - Middle Aged MH - Multicenter Studies as Topic/*statistics & numerical data MH - Neoplasm Metastasis MH - Oral Hygiene MH - Osteonecrosis/*chemically induced/epidemiology/prevention & control MH - Paclitaxel/administration & dosage MH - Prospective Studies MH - Randomized Controlled Trials as Topic/*statistics & numerical data MH - Taxoids/administration & dosage MH - Vinblastine/administration & dosage/analogs & derivatives EDAT- 2010/04/03 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/04/03 06:00 PHST- 2009/12/24 [received] PHST- 2010/03/18 [accepted] PHST- 2010/04/02 [aheadofprint] AID - 10.1007/s10549-010-0866-3 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):181-8. Epub 2010 Apr 2. PMID- 20349271 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101101 IS - 1573-7225 (Electronic) IS - 0957-5243 (Linking) VI - 21 IP - 8 DP - 2010 Aug TI - Phenotypic characterization and risk factors for interval breast cancers in a population-based breast cancer screening program in Barcelona, Spain. PG - 1155-64 AB - OBJECTIVE: To analyze phenotypic classification and other risk factors for interval breast cancer, focusing on true interval and false negative cancers. METHODS: A nested case-control study was performed among 115 cancers detected between two screening mammograms (interval cancers) and 115 screen-detected cancers diagnosed between 1995 and 2008 in a population-based breast cancer screening program in Barcelona (Spain). Bivariate and multivariate analyses were performed to compare patient and tumor molecular characteristics among all interval cancers, true intervals and false negatives, and screen-detected cancers. RESULTS: A total of 42.5% of interval cancers were true interval tumors and 16.2% were false negatives. High breast density and triple negative phenotype were more frequent in true interval cancers than in screen-detected cancers (57.6 and 34.1%, respectively for breast density, p = 0.023; 28.1 and 7.5%, respectively for triple negative phenotype, p = 0.028), while no statistically significant differences were observed between false negatives and screen-detected cancers. The main adjusted factors associated with true interval cancers compared with screen-detected cancers were high breast density and triple negative phenotype (OR = 3.1, 95% CI, 1.03-9.24 and OR = 8.9, 95% CI, 2.03-38.62, respectively). CONCLUSION: A more aggressive molecular phenotype and high breast density were identified in breast tumors that truly arise in the interval between screenings. AD - Evaluation and Clinical Epidemiology Department, Hospital del Mar-IMIM, Passeig Maritim, 25-29, 08003 Barcelona, Spain. FAU - Domingo, Laia AU - Domingo L FAU - Sala, Maria AU - Sala M FAU - Servitja, Sonia AU - Servitja S FAU - Corominas, Josep Maria AU - Corominas JM FAU - Ferrer, Francisco AU - Ferrer F FAU - Martinez, Juan AU - Martinez J FAU - Macia, Francesc AU - Macia F FAU - Quintana, Maria Jesus AU - Quintana MJ FAU - Albanell, Joan AU - Albanell J FAU - Castells, Xavier AU - Castells X LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100328 PL - Netherlands TA - Cancer Causes Control JT - Cancer causes & control : CCC JID - 9100846 SB - IM MH - Aged MH - Breast Neoplasms/epidemiology/*pathology/prevention & control MH - Case-Control Studies MH - Early Detection of Cancer/methods MH - Female MH - Humans MH - Immunohistochemistry MH - Mammography MH - Middle Aged MH - Phenotype MH - Risk Factors MH - Spain/epidemiology EDAT- 2010/03/30 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/03/30 06:00 PHST- 2009/12/21 [received] PHST- 2010/03/10 [accepted] PHST- 2010/03/28 [aheadofprint] AID - 10.1007/s10552-010-9541-6 [doi] PST - ppublish SO - Cancer Causes Control. 2010 Aug;21(8):1155-64. Epub 2010 Mar 28. PMID- 20309626 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Transforming growth factor-beta1 polymorphisms and breast cancer risk: a meta-analysis based on 27 case-control studies. PG - 273-9 AB - The association between transforming growth factor-beta1 (TGF-beta1) gene polymorphisms and breast cancer risk has been widely reported, but results were somewhat controversial and underpowered. To derive a more precise estimation of the relationship between TGF-beta1 polymorphisms and breast cancer risk, we conducted a meta-analysis of all available case-control studies relating the T869C and/or C-509T polymorphisms of the TGF-beta1 gene to the risk of developing breast cancer. Eligible articles were identified by search of databases including MEDLINE, PubMed, Web of Science, EMBASE, and Chinese Biomedical Literature database (CBM) for the period up to March 2010. Finally, a total of 17 articles involving 27 case-control studies were identified, 25 with 20,022 cases and 24,423 controls for T869C polymorphism and eight with 10,633 cases and 13,648 controls for C-509T polymorphism. The pooled ORs were performed for the allele contrasts, additive genetic model, dominant genetic model and recessive genetic model, respectively. Subgroup analysis was also performed by ethnicity for T869C polymorphism. With respect to T869C polymorphism, no association was found in overall analysis (C vs. T: OR = 1.033, 95% CI = 0.996-1.072). In the subgroup analysis by ethnicity, significantly increased risk was found in Caucasian population (C vs. T: OR = 1.051, 95% CI = 1.018-1.085; CC vs. TT + TC: OR = 1.083, 95% CI = 1.019-1.151), but not in Asian population (C vs. T: OR = 1.054, 95% CI = 0.983-1.130). With respect to C-509T polymorphism, no significant association with breast cancer risk was demonstrated in overall analysis (T vs. C: OR = 0.986, 95% CI = 0.936-1.039). It can be concluded that potentially functional TGF-Beta1 T869C polymorphism may play a low penetrance role in breast cancer susceptibility in an ethnicity-specific manner. AD - Breast Disease Center, Southwest Hospital, Third Military Medical University, Gaotanyan Street 29, Chongqing 400038, China. FAU - Qi, Xiaowei AU - Qi X FAU - Zhang, Fan AU - Zhang F FAU - Yang, Xinhua AU - Yang X FAU - Fan, Linjun AU - Fan L FAU - Zhang, Yi AU - Zhang Y FAU - Chen, Li AU - Chen L FAU - Zhou, Yan AU - Zhou Y FAU - Chen, Xianchun AU - Chen X FAU - Zhong, Ling AU - Zhong L FAU - Jiang, Jun AU - Jiang J LA - eng PT - Comparative Study PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100323 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Transforming Growth Factor beta1) SB - IM MH - Amino Acid Substitution MH - Asian Continental Ancestry Group/genetics/statistics & numerical data MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Ethnic Groups/genetics/statistics & numerical data MH - European Continental Ancestry Group/genetics/statistics & numerical data MH - Exons/genetics MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Menopause MH - Models, Genetic MH - Odds Ratio MH - Penetrance MH - *Polymorphism, Single Nucleotide MH - Risk MH - Transforming Growth Factor beta1/*genetics EDAT- 2010/03/24 06:00 MHDA- 2010/10/26 06:00 CRDT- 2010/03/24 06:00 PHST- 2010/03/07 [received] PHST- 2010/03/10 [accepted] PHST- 2010/03/23 [aheadofprint] AID - 10.1007/s10549-010-0847-6 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):273-9. Epub 2010 Mar 23. PMID- 20229034 OWN - NLM STAT- MEDLINE DA - 20100924 DCOM- 20101027 IS - 1432-1335 (Electronic) IS - 0171-5216 (Linking) VI - 136 IP - 11 DP - 2010 Nov TI - Evaluation of protein pigment epithelium-derived factor (PEDF) and microvessel density (MVD) as prognostic indicators in breast cancer. PG - 1719-27 AB - PURPOSE: Angiogenesis, which plays an important role in tumor growth and metastasis, is regulated by a balance between angiogenic stimulators and inhibitors. Pigment epithelium-derived factor (PEDF), a secreted glycoprotein is an important inhibitor of angiogenesis. Although the precise mechanisms by which PEDF exerts its actions remain poorly understood, there is growing evidence supporting the role of PEDF as a candidate antitumor agent. In this study, we investigated the role of PEDF in breast cancer. METHODS: We investigated the correlation of PEDF protein levels with cancer progression and prognosis in patients with invasive ductal breast cancer (IDC). We used immunohistochemistry in a cohort of 119 breast cancer patients to examine the expression of PEDF protein with an anti-PEDF antibody and to measure the microvessel density (MVD) with an anti-CD34 antibody. RESULTS: PEDF was an endogenous inhibitor of angiogenesis in endothelial cells. Decreased intratumoral expression of PEDF was associated with a higher microvessel density (MVD), a more metastatic phenotype, and poorer clinical outcome. PEDF was positive in 43.7% patients. Patients with low PEDF expression had a significantly higher MVD count when compared with patients with high PEDF expression. In univariate and multivariate analysis, PEDF was an independent prognostic factor. CONCLUSION: The inverse correlation between PEDF expression and MVD in human breast cancer suggests that low PEDF expression is associated with angiogenesis in breast cancer. PEDF expression is therefore a potentially useful prognostic marker for breast cancer. AD - Department of Breast Surgery, Tumor Hospital, Harbin Medical University, 158 HaPing Road, Harbin 150081, China. FAU - Zhou, Dan AU - Zhou D FAU - Cheng, Shao-Qiang AU - Cheng SQ FAU - Ji, Hong-Fei AU - Ji HF FAU - Wang, Jin-Song AU - Wang JS FAU - Xu, Hai-Tao AU - Xu HT FAU - Zhang, Guo-Qiang AU - Zhang GQ FAU - Pang, Da AU - Pang D LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100313 PL - Germany TA - J Cancer Res Clin Oncol JT - Journal of cancer research and clinical oncology JID - 7902060 RN - 0 (Eye Proteins) RN - 0 (Nerve Growth Factors) RN - 0 (Serpins) RN - 0 (pigment epithelium-derived factor) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Breast Neoplasms/blood supply/metabolism/mortality/*pathology MH - Cohort Studies MH - Disease Progression MH - Eye Proteins/*genetics/metabolism MH - Female MH - Gene Expression Regulation, Neoplastic MH - Humans MH - Immunohistochemistry MH - *Microcirculation MH - Middle Aged MH - Neoplasm Metastasis/pathology MH - Neoplasm Staging MH - Neovascularization, Pathologic/metabolism/*pathology MH - Nerve Growth Factors/*genetics/metabolism MH - Prognosis MH - Serpins/*genetics/metabolism MH - Survival Analysis MH - Survival Rate EDAT- 2010/03/17 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/03/16 06:00 PHST- 2009/10/09 [received] PHST- 2010/02/08 [accepted] PHST- 2010/03/13 [aheadofprint] AID - 10.1007/s00432-010-0830-y [doi] PST - ppublish SO - J Cancer Res Clin Oncol. 2010 Nov;136(11):1719-27. Epub 2010 Mar 13. PMID- 20204407 OWN - NLM STAT- MEDLINE DA - 20100924 DCOM- 20101027 IS - 1432-1335 (Electronic) IS - 0171-5216 (Linking) VI - 136 IP - 11 DP - 2010 Nov TI - Comparison of microarray-based RNA expression with ELISA-based protein determination of HER2, uPA and PAI-1 in tumour tissue of patients with breast cancer and relation to outcome. PG - 1709-18 AB - PURPOSE: Prognostic and predictive markers in breast cancer are currently determined by single analysis of protein amounts. If RNA-based multi-gene analyses enter clinical practice, simultaneous determination of currently established markers like human epidermal growth factor receptor 2 (HER2), urokinase plasminogen activator (uPA) and its inhibitor (PAI-1) would represent an elegant simplification. To investigate the correlation between RNA and protein levels, we assessed HER2, uPA and PAI-1 in patients with breast cancer. In addition, we evaluated the influence of these factors on patient outcome. METHODS: We collected tumour samples from 133 patients with primary breast cancer. Protein and mRNA levels were measured for HER2, uPA and PAI-1. Protein concentration was measured by ELISA, mRNA expression was analysed by Affymetrix A133U Gene Chip and validated by quantitative PCR. RESULTS: We were able to demonstrate a statistically significant correlation between mRNA and protein expression for HER2 (r = 0.67, P < 0.001) and uPA (r = 0.7, P < 0.001) but not for PAI-1 (r = 0.27). We observed a prognostic information for PAI-1 mRNA and protein values. Patients with high PAI-1 mRNA expression had a reduced 10-year disease-free survival (DFS) rate (60 vs. 70%, P = 0.071) and 10-year overall survival (OS) rate (68 vs. 79%, P = 0.034). Patients with PAI-1 protein levels above 14 ng/mg protein had a reduced disease-free (10-year DFS rate 54 vs. 71%, P = 0.006) and overall survival rate (10-year OS-rate 63 vs. 83%, P = 0.018). In the patient cohort with no chemotherapy, PAI-1 mRNA levels were the strongest prognostic factor for OS in univariate and multivariate analysis. CONCLUSIONS: Results of RNA-based multi-gene analyses of the prognostic and predictive markers HER2 and uPA correlate with the corresponding protein levels. This is not the case for PAI-1. However, PAI-1 mRNA expression might reveal new clinically relevant information in addition to PAI protein levels. AD - Department of Gynecology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. FAU - Witzel, Isabell D AU - Witzel ID FAU - Milde-Langosch, Karin AU - Milde-Langosch K FAU - Wirtz, Ralph M AU - Wirtz RM FAU - Roth, Claudia AU - Roth C FAU - Ihnen, Maike AU - Ihnen M FAU - Mahner, Sven AU - Mahner S FAU - Zu Eulenburg, Christine AU - Zu Eulenburg C FAU - Janicke, Fritz AU - Janicke F FAU - Muller, Volkmar AU - Muller V LA - eng PT - Journal Article DEP - 20100304 PL - Germany TA - J Cancer Res Clin Oncol JT - Journal of cancer research and clinical oncology JID - 7902060 RN - 0 (DNA Primers) RN - 0 (DNA Probes) RN - 0 (Plasminogen Activator Inhibitor 1) RN - 0 (RNA, Messenger) RN - 0 (RNA, Neoplasm) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - EC 2.7.10.1 (ERBB2 protein, human) RN - EC 2.7.10.1 (Receptor, erbB-2) RN - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) SB - IM MH - Breast Neoplasms/drug therapy/*genetics/mortality/pathology/radiotherapy MH - Combined Modality Therapy MH - DNA Primers MH - DNA Probes MH - Disease-Free Survival MH - Enzyme-Linked Immunosorbent Assay MH - Female MH - Gene Amplification MH - Gene Expression Regulation, Neoplastic MH - Humans MH - *Oligonucleotide Array Sequence Analysis MH - Plasminogen Activator Inhibitor 1/*genetics MH - Polymerase Chain Reaction MH - Prognosis MH - RNA, Messenger/*genetics MH - RNA, Neoplasm/*genetics MH - Receptor, erbB-2/*genetics MH - Receptors, Estrogen/analysis MH - Receptors, Progesterone/analysis MH - Survival Rate MH - Treatment Outcome MH - Urokinase-Type Plasminogen Activator/*genetics EDAT- 2010/03/06 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/03/06 06:00 PHST- 2009/10/04 [received] PHST- 2010/02/08 [accepted] PHST- 2010/03/04 [aheadofprint] AID - 10.1007/s00432-010-0829-4 [doi] PST - ppublish SO - J Cancer Res Clin Oncol. 2010 Nov;136(11):1709-18. Epub 2010 Mar 4. PMID- 20177704 OWN - NLM STAT- MEDLINE DA - 20100924 DCOM- 20101027 IS - 1432-1335 (Electronic) IS - 0171-5216 (Linking) VI - 136 IP - 11 DP - 2010 Nov TI - Alterations in p53, BRCA1, ATM, PIK3CA, and HER2 genes and their effect in modifying clinicopathological characteristics and overall survival of Bulgarian patients with breast cancer. PG - 1657-69 AB - PURPOSE: Though p53, BRCA1, ATM, PIK3CA, and HER2 genes are shown to be involved in various aspects of breast carcinogenesis, their functional relationship and clinical value are still disputable. We investigated the genetic status or expression profile of these genes to further elucidate their clinical significance. METHODS: PCR-SSCP-Sequencing of p53, BRCA1, ATM, and PIK3CA was performed in 145 Bulgarian patients with sporadic breast cancer. Expression profiles of HER2 were determined by ICH and CISH. Relationship between mutations and clinicopathological characteristics was evaluated by Chi-squared and Fisher's exact tests. Multivariate Cox proportional hazard test and Kaplan-Meier analysis were used to evaluate differences in overall survival between groups. RESULTS: The frequency of p53 (22.07%), BRCA1 (0.69%), ATM (7.59%), and PIK3CA (31.25%) alterations and HER2 (21.21%) overexpression was estimated. Mutated p53 was associated with tumor size (P = 0.033) and grade of malignancy (P = 0.001), ATM--with grade of malignancy (P = 0.032), and PIK3CA--with PR-positive tumors (P = 0.047). HER2 overexpression correlated with age of diagnosis (P = 0.009), tumor size (P = 0.0004), and ER expression (P = 0.011). Univariate survival analysis showed that mutated p53 is an indicator for worse outcome (P = 0.041). Combination of two genetic abnormalities did not correlate with more aggressive carcinogenesis and worse overall survival. CONCLUSIONS: Our data indicated that p53, BRCA1, ATM, PIK3CA, and HER2 alterations specifically correlate with clinicopathological characteristics of Bulgarian patients with breast cancer. Of these genes, only mutated p53 showed significant, though not independent, negative effect on overall survival. AD - Institute of Genetics Akad. Doncho Kostoff, Department of Molecular Genetics, Bulgarian Academy of Sciences, Plovdivsko shosse 13 km., 1113 Sofia, Bulgaria. FAU - Bozhanov, Stefan S AU - Bozhanov SS FAU - Angelova, Svetla G AU - Angelova SG FAU - Krasteva, Maria E AU - Krasteva ME FAU - Markov, Tsanko L AU - Markov TL FAU - Christova, Svetlana L AU - Christova SL FAU - Gavrilov, Ivan G AU - Gavrilov IG FAU - Georgieva, Elena I AU - Georgieva EI LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100223 PL - Germany TA - J Cancer Res Clin Oncol JT - Journal of cancer research and clinical oncology JID - 7902060 RN - 0 (BRCA1 Protein) RN - 0 (Cell Cycle Proteins) RN - 0 (DNA, Neoplasm) RN - 0 (DNA-Binding Proteins) RN - 0 (HER2 protein, human) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Suppressor Proteins) RN - EC 2.7.1.137 (1-Phosphatidylinositol 3-Kinase) RN - EC 2.7.1.137 (PIK3CA protein, human) RN - EC 2.7.1.37 (ataxia telangiectasia mutated protein) RN - EC 2.7.10.1 (Receptor, erbB-2) RN - EC 2.7.11.1 (Protein-Serine-Threonine Kinases) SB - IM MH - 1-Phosphatidylinositol 3-Kinase/*genetics MH - BRCA1 Protein/*genetics MH - Breast Neoplasms/*genetics/mortality/pathology MH - Bulgaria MH - Cell Cycle Proteins/*genetics MH - DNA, Neoplasm/genetics/isolation & purification MH - DNA-Binding Proteins/*genetics MH - Exons/genetics MH - Female MH - Gene Expression Profiling MH - *Genes, erbB-2 MH - *Genes, p53 MH - Humans MH - Introns/genetics MH - Lymphatic Metastasis/genetics MH - Polymerase Chain Reaction MH - Prognosis MH - Proportional Hazards Models MH - Protein-Serine-Threonine Kinases/*genetics MH - Receptor, erbB-2/*genetics MH - Receptors, Estrogen/genetics MH - Receptors, Progesterone/genetics MH - Survivors MH - Tumor Suppressor Proteins/*genetics EDAT- 2010/02/24 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/02/24 06:00 PHST- 2009/06/18 [received] PHST- 2010/02/04 [accepted] PHST- 2010/02/23 [aheadofprint] AID - 10.1007/s00432-010-0824-9 [doi] PST - ppublish SO - J Cancer Res Clin Oncol. 2010 Nov;136(11):1657-69. Epub 2010 Feb 23. PMID- 20162609 OWN - NLM STAT- MEDLINE DA - 20100927 DCOM- 20101104 IS - 1097-0215 (Electronic) IS - 0020-7136 (Linking) VI - 127 IP - 10 DP - 2010 Nov 15 TI - Population-based breast (female) and cervix cancer rates in the Gambia: evidence of ethnicity-related variations. PG - 2248-56 AB - Since 1987, the Gambia National Cancer Registry has provided nationwide cancer registration for the Gambia. We used data from 1998 to 2006 to assess age-standardized incidence rates (ASRs) of 2 common cancers in women, breast and cervix. With an ASR of 15.42 (95% CI [14.18-16.66]) for cervix and 5.86 (95% CI [5.12-6.59]) for breast per 10(5) person-years, these cancers ranked first and third, respectively, among Gambian women (the second most common being liver, ASR 14.90). Incidence of both cancers, breast and cervix, increased rapidly at young ages to reach a peak at ages 40-44 years. Significant differences were observed in relation to ethnicity. Using the Mandinka (42% of the population) as a reference, breast cancer incidence rates were 2.16-fold higher (95% CI [1.33-3.52]) in Jola (10% of the population), specially at early-onset ages (before 40 years). For cervix cancer, highest rates were observed in Fula (18% of the population; risk ratio (RR): 1.84 (95% CI [1.44-2.36])). In contrast, a significantly lower risk was observed in the Serrahuleh (9% of the population; RR: 0.54 (95% CI [0.31-0.96]). This study revealed a preponderance of early-onset breast cancer among Gambian women similar to that seen in African women in more developed countries but also demonstrates large ethnic variations. It points to the need for further studies on cancer determinants to improve prevention, early detection and therapeutic management of these diseases in a low-resource setting in West Africa. AD - International Agency for Research on Cancer, 150 cours Albert Thomas, Lyon, France. FAU - Sighoko, Dominique AU - Sighoko D FAU - Bah, Ebrima AU - Bah E FAU - Haukka, Jari AU - Haukka J FAU - McCormack, Valerie A AU - McCormack VA FAU - Aka, Elizabeth Patu AU - Aka EP FAU - Bourgeois, Denis AU - Bourgeois D FAU - Autier, Philippe AU - Autier P FAU - Byrnes, Graham AU - Byrnes G FAU - Curado, Maria Paula AU - Curado MP FAU - Hainaut, Pierre AU - Hainaut P LA - eng PT - Journal Article PL - United States TA - Int J Cancer JT - International journal of cancer. Journal international du cancer JID - 0042124 SB - IM MH - Adult MH - Age Factors MH - Aged MH - Breast Neoplasms/*epidemiology/ethnology MH - Female MH - Gambia/epidemiology MH - Humans MH - Incidence MH - Middle Aged MH - Registries MH - Uterine Cervical Neoplasms/*epidemiology/ethnology MH - Young Adult EDAT- 2010/02/18 06:00 MHDA- 2010/11/05 06:00 CRDT- 2010/02/18 06:00 AID - 10.1002/ijc.25244 [doi] PST - ppublish SO - Int J Cancer. 2010 Nov 15;127(10):2248-56. PMID- 20151215 OWN - NLM STAT- MEDLINE DA - 20100708 DCOM- 20101027 IS - 1534-4681 (Electronic) IS - 1068-9265 (Linking) VI - 17 IP - 8 DP - 2010 Aug TI - Micrometastatic node-positive breast cancer: long-term outcomes and identification of high-risk subsets in a large population-based series. PG - 2138-46 AB - PURPOSE: The prognostic implication of breast cancer with nodal micrometastases measuring >0.2 mm but < or =2 mm (pNmic) is unclear. This study evaluates survival in pNmic relative to node-negative (N0) and macroscopic node-positive (pNmac) disease in a large population-based series. METHODS: Subjects were 9,637 women diagnosed between 1989 and 1999, referred to the British Columbia Cancer Agency with pT1-2, node-negative and node-positive, M0 breast cancer. Kaplan-Meier breast-cancer-specific survival (BCSS) and overall survival (OS) were compared between patients with pN0 (n = 7,988), pNmic (n = 491), and pNmac disease (n = 1,158), according to the number of positive nodes and the lymph node ratio (LNR) of positive to excised nodes. Cox regression and recursive partitioning analyses were performed to identify significant factors associated with survival. RESULTS: Median follow-up was 8.2 years. Patients with pNmic disease had significantly poorer outcomes compared with pN0 cancers, with progressively lower BCSS and OS with increasing number of positive nodes and with LNR > 0.25. On multivariable analysis, histologic subtype, T stage, number of positive nodes, LNR, grade, lymphovascular invasion, estrogen receptor status, and systemic therapy use were factors significantly associated with BCSS and OS. Recursive partitioning trees for BCSS and OS both selected the pN/LNR variable at the first split, indicating that this variable provided the strongest prognostic separation. CONCLUSION: Patients with nodal micrometastases are a heterogeneous population with varying breast cancer mortality risks. The number of positive nodes and the LNR should be considered in conjunction with tumor factors in risk estimates and treatment decisions for patients with nodal micrometastatic breast cancer. AD - Breast Cancer Outcomes Unit, British Columbia Cancer Agency, Victoria, BC, Canada. ptruong@bccancer.bc.ca FAU - Truong, Pauline T AU - Truong PT FAU - Lesperance, Mary AU - Lesperance M FAU - Li, Karen Hui AU - Li KH FAU - MacFarlane, Robyn AU - MacFarlane R FAU - Speers, Caroline H AU - Speers CH FAU - Chia, Stephen AU - Chia S LA - eng PT - Journal Article DEP - 20100212 PL - United States TA - Ann Surg Oncol JT - Annals of surgical oncology JID - 9420840 SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Breast Neoplasms/*mortality/*pathology MH - Case-Control Studies MH - Female MH - Follow-Up Studies MH - Humans MH - Kaplan-Meiers Estimate MH - Lymph Node Excision MH - Lymph Nodes/*pathology/surgery MH - Lymphatic Metastasis MH - Middle Aged MH - Prognosis MH - Proportional Hazards Models MH - Regression Analysis MH - Risk Assessment MH - Survival Analysis MH - Young Adult EDAT- 2010/02/13 06:00 MHDA- 2010/10/28 06:00 CRDT- 2010/02/13 06:00 PHST- 2009/11/14 [received] PHST- 2010/02/12 [aheadofprint] AID - 10.1245/s10434-010-0954-y [doi] PST - ppublish SO - Ann Surg Oncol. 2010 Aug;17(8):2138-46. Epub 2010 Feb 12. PMID- 20130984 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Mammographic density does not differ between unaffected BRCA1/2 mutation carriers and women at low-to-average risk of breast cancer. PG - 245-55 AB - Elevated mammographic density (MD) is one of the strongest risk factors for sporadic breast cancer. Epidemiologic evidence suggests that MD is, in part, genetically determined; however, the relationship between MD and BRCA1/2 mutation status is equivocal. We compared MD in unaffected BRCA1/2 mutation carriers enrolled in the U.S. National Cancer Institute's Clinical Genetics Branch's Breast Imaging Study (n = 143) with women at low-to-average breast cancer risk enrolled in the same study (n = 29) or the NCI/National Naval Medical Center's Susceptibility to Breast Cancer Study (n = 90). The latter were BRCA mutation-negative members of mutation-positive families or women with no prior breast cancer, a Pedigree Assessment Tool score <8 (i.e., low risk of a hereditary breast cancer syndrome) and a Gail score <1.67. A single experienced mammographer measured MD using a computer-assisted thresholding method. We collected standard breast cancer risk factor information in both studies. Unadjusted mean percent MD was higher in women with BRCA1/2 mutations compared with women at low-to-average breast cancer risk (37.3% vs. 33.4%; P = 0.04), but these differences disappeared after adjusting for age and body mass index (34.9% vs. 36.3%; P = 0.43). We explored age at menarche, nulliparity, age at first birth, menopausal status, number of breast biopsies, and exposure to exogenous hormonal agents as potential confounders of the MD and BRCA1/2 association. Taking these factors into account did not significantly alter the results of the age/body mass index-adjusted analysis. Our results do not provide support for an independent effect of BRCA1/2 mutation status on mammographic density. AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, Office of Preventive Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. gierachg@mail.nih.gov FAU - Gierach, Gretchen L AU - Gierach GL FAU - Loud, Jennifer T AU - Loud JT FAU - Chow, Catherine K AU - Chow CK FAU - Prindiville, Sheila A AU - Prindiville SA FAU - Eng-Wong, Jennifer AU - Eng-Wong J FAU - Soballe, Peter W AU - Soballe PW FAU - Giambartolomei, Claudia AU - Giambartolomei C FAU - Mai, Phuong L AU - Mai PL FAU - Galbo, Claudia E AU - Galbo CE FAU - Nichols, Kathryn AU - Nichols K FAU - Calzone, Kathleen A AU - Calzone KA FAU - Vachon, Celine AU - Vachon C FAU - Gail, Mitchell H AU - Gail MH FAU - Greene, Mark H AU - Greene MH LA - eng GR - N02-CP-11019-50/CP/NCI NIH HHS/United States GR - N02-CP-65504-50/CP/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20100204 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 SB - IM MH - Adult MH - Breast Neoplasms/*genetics/*radiography MH - Female MH - Genes, BRCA1 MH - Genes, BRCA2 MH - Genetic Predisposition to Disease MH - Humans MH - Image Interpretation, Computer-Assisted MH - *Mammography MH - Middle Aged MH - Mutation MH - Risk Factors EDAT- 2010/02/05 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/02/05 06:00 PHST- 2010/01/11 [received] PHST- 2010/01/13 [accepted] PHST- 2010/02/04 [aheadofprint] AID - 10.1007/s10549-010-0749-7 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):245-55. Epub 2010 Feb 4. PMID- 20130981 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - COMT Val158Met polymorphism and breast cancer risk: evidence from 26 case-control studies. PG - 265-70 AB - The Catechol-O-methyltransferase (COMT) plays an important role in the development of breast cancer. Many previous epidemiologic studies explored the association of COMT Val158Met polymorphism with breast cancer susceptibility. However, the results were inconsistent. We therefore performed a meta-analysis of 26 published studies including 16,693 breast cancer patients and 18,261 healthy controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association of the COMT Val158Met polymorphism with breast cancer risk. No significant association was found in all genetic models in overall, Asian, European populations. After the studies whose genotype frequencies in the controls did not fulfill Hardy-Weinberg equilibrium were excluded, we found a borderline significant decreased breast cancer risk among Europeans (for the recessive model LL versus HH/HL: OR = 0.90, 95% CI = 0.90-1.00, P (heterogeneity) = 0.33). There was no between-study heterogeneity. In conclusion, COMT Val158Met polymorphism may be a low-penetrant risk factor for breast cancer development in European population. AD - Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, 210029 Nanjing, China. dhxnjmu@126.com FAU - Ding, Haixia AU - Ding H FAU - Fu, Yuanyuan AU - Fu Y FAU - Chen, Weixian AU - Chen W FAU - Wang, Zhanwei AU - Wang Z LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20100204 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 2.1.1.6 (Catechol O-Methyltransferase) SB - IM MH - Asian Continental Ancestry Group/genetics MH - Breast Neoplasms/*genetics MH - Case-Control Studies MH - Catechol O-Methyltransferase/genetics MH - European Continental Ancestry Group/genetics MH - Female MH - Genetic Predisposition to Disease/*genetics MH - Humans MH - Odds Ratio MH - Penetrance MH - Polymorphism, Single Nucleotide/*genetics MH - Risk Factors EDAT- 2010/02/05 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/02/05 06:00 PHST- 2010/01/18 [received] PHST- 2010/01/19 [accepted] PHST- 2010/02/04 [aheadofprint] AID - 10.1007/s10549-010-0759-5 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):265-70. Epub 2010 Feb 4. PMID- 20127279 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - XRCC2 Arg188His polymorphism is not directly associated with breast cancer risk: evidence from 37,369 subjects. PG - 219-25 AB - Several common single-nucleotide polymorphisms (SNPs) within the XRCC2 gene have been identified as potential breast cancer susceptibility loci and a coding SNP in exon 3 (Arg188His, rs3218536) has been extensively studied, though the results were inconclusive. We, in this study, performed a more convincing and precise estimation of the relationship between Arg188His and breast cancer by meta-analyzing the currently available evidence from literature. A total of 16 studies involving 18,341 cases and 19,028 controls (37,369 subjects) were identified for meta-analysis. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association in the codominant model, dominant model, and recessive model. When all the studies were pooled into meta-analysis, there was no evidence of a significant association between Arg188His and breast cancer risk in any genetic models. Notably, Arg188His tended to be related to breast cancer in a fixed-effects, dominant model (OR = 0.922, 95% CI: 0.870-0.978, P = 0.007); however, since there was a between-study heterogeneity (P (h) = 0.014), we assessed the association using a random-effects model instead and no significance was observed (OR = 0.932, 95% CI: 0.852-1.020, P = 0.128). Subgroup analysis by ethnicity did not change the results. In summary, the present meta-analysis suggests that the XRCC2 Arg188His is not directly associated with breast cancer risk. However, considering that susceptibility is likely to be the result of a complex interplay between genetic variation and environmental factors, we cannot rule out the possibility of interactions between Arg188His and other variants. Further investigation on the influence of this SNP in modifying the relationship between environment exposures and breast cancer risk is still needed. AD - Department of Breast Surgery, Cancer Hospital/Cancer Institute, Breast Cancer Institute, Fudan University, 399 Ling-Ling Road, 200032 Shanghai, People's Republic of China. FAU - Yu, Ke-Da AU - Yu KD FAU - Chen, Ao-Xiang AU - Chen AX FAU - Qiu, Li-Xin AU - Qiu LX FAU - Fan, Lei AU - Fan L FAU - Yang, Chen AU - Yang C FAU - Shao, Zhi-Ming AU - Shao ZM LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100202 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (DNA-Binding Proteins) RN - 0 (XRCC2 protein, human) SB - IM MH - Breast Neoplasms/*genetics MH - DNA-Binding Proteins/*genetics MH - Female MH - Genetic Predisposition to Disease/*genetics MH - Humans MH - Odds Ratio MH - Polymorphism, Single Nucleotide/*genetics MH - Risk Factors EDAT- 2010/02/04 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/02/04 06:00 PHST- 2010/01/13 [received] PHST- 2010/01/18 [accepted] PHST- 2010/02/02 [aheadofprint] AID - 10.1007/s10549-010-0753-y [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):219-25. Epub 2010 Feb 2. PMID- 20127278 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - The association between ERCC2 Asp312Asn polymorphism and breast cancer risk: a meta-analysis involving 22,766 subjects. PG - 227-31 AB - To date, many publications discussed the correlation between ERCC2 Asp312Asn polymorphism and breast cancer risk. However, the results were not unanimous. In order to derive a more precise conclusion, a meta-analysis was performed in this study by searching Medline, PubMed, and ISI Web of Knowledge databases. Finally, 17 studies including 12,019 cases and 10,747 controls were collected for this meta-analysis. The strength of association between ERCC2 Asp312Asn polymorphism and breast cancer risk was assessed by calculating crude ORs with 95% CIs. Overall, no significant associations between ERCC2 Asp312Asn polymorphism and breast cancer susceptibility were found. In the stratified analysis by ethnicity, significant associations were observed for Asn/Asn versus Asp/Asp (OR = 0.55; 95% CI 0.32-0.96) and Asn/Asn versus Asn/Asp + Asp/Asp (OR = 0.53; 95% CI 0.32-0.90) in Asians. In the stratified analysis by study design, significant associations were found for Asn/Asn versus Asp/Asp (OR = 0.79; 95% CI 0.64-0.98) and Asn/Asn versus Asn/Asp + Asp/Asp (OR = 0.82; 95% CI 0.68-0.99) in population-based studies. In conclusion, this meta-analysis provides an evidence that ERCC2 312Asn allele may have a protective effect for breast cancer development in Asians. AD - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, People's Republic of China. FAU - Yao, Lei AU - Yao L FAU - Qiu, Li-Xin AU - Qiu LX FAU - Yu, Lu AU - Yu L FAU - Yang, Zhen AU - Yang Z FAU - Yu, Xia-Jia AU - Yu XJ FAU - Zhong, Yang AU - Zhong Y FAU - Hu, Xi-Chun AU - Hu XC FAU - Yu, Long AU - Yu L LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100202 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 5.99.- (ERCC2 protein, human) RN - EC 5.99.- (Xeroderma Pigmentosum Group D Protein) SB - IM MH - Asian Continental Ancestry Group/genetics MH - Breast Neoplasms/*genetics MH - Female MH - Genetic Predisposition to Disease/*genetics MH - Humans MH - Polymorphism, Single Nucleotide/*genetics MH - Risk Factors MH - Xeroderma Pigmentosum Group D Protein/*genetics EDAT- 2010/02/04 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/02/04 06:00 PHST- 2010/01/13 [received] PHST- 2010/01/18 [accepted] PHST- 2010/02/02 [aheadofprint] AID - 10.1007/s10549-010-0754-x [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):227-31. Epub 2010 Feb 2. PMID- 20122741 OWN - NLM STAT- MEDLINE DA - 20100712 DCOM- 20101029 IS - 1573-2517 (Electronic) IS - 0165-0327 (Linking) VI - 124 IP - 3 DP - 2010 Aug TI - Depression and serotonin transporter (5-HTTLPR) polymorphism in breast cancer patients. PG - 346-50 AB - BACKGROUND: Mixed evidence in the general population and medically ill patients has suggested that homozygous carriers of the short allele (s/s) of the serotonin transporter gene-linked polymorphic region (5-HTTLPR) may increase the risk of depression in comparison with carriers of the long allele (l/l) or s/l. Given the lack of data in oncology, we examined the relationship of depression with the 5-HTTLPR and psychosocial variables among breast cancer patients. METHODS: A sample of 145 breast cancer patients were studied as regards to depression, psychosocial-related variables (coping, Type D-personality, life events, and social support), and the 5-HTTLPR, which was genotyped by using a standard protocol with DNA extracted from the blood. RESULTS: No difference was found between s/s, s/l and l/l patients on depression and any other psychosocial variable. No gene-by environment (GxE) interactions were observed between the 5-HTTLPR and recent life events. CONCLUSIONS: The study did not provide support of a possible association between 5-HTTLPR polymorphism, alone or in conjunction with life events, and depression in newly diagnosed breast cancer. Further follow-up studies are however necessary to confirm these data. CI - Copyright 2009. Published by Elsevier B.V. AD - Section of Psychiatry, Department of Behavior and Communication, University of Ferrara and Unit of Clinical Psychiatry Department of Mental Health and Drug Abuse, Health Agency, NHS, Ferrara, Italy. luigi.grassi@unife.it FAU - Grassi, Luigi AU - Grassi L FAU - Rossi, Elena AU - Rossi E FAU - Cobianchi, Marina AU - Cobianchi M FAU - Aguiari, Letizia AU - Aguiari L FAU - Capozzo, Marianna AU - Capozzo M FAU - Martinis, Elisabetta AU - Martinis E FAU - Nanni, Maria Giulia AU - Nanni MG FAU - Lelli, Giorgio AU - Lelli G FAU - Schillani, Giulia AU - Schillani G FAU - Biancosino, Bruno AU - Biancosino B FAU - Giraldi, Tullio AU - Giraldi T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100131 PL - Netherlands TA - J Affect Disord JT - Journal of affective disorders JID - 7906073 RN - 0 (SLC6A4 protein, human) RN - 0 (Serotonin Plasma Membrane Transport Proteins) SB - IM MH - Adaptation, Psychological MH - Adult MH - Aged MH - *Alleles MH - Breast Neoplasms/*genetics/*psychology MH - Female MH - Genetic Predisposition to Disease/genetics/psychology MH - Genotype MH - Heterozygote Detection MH - Humans MH - Life Change Events MH - Middle Aged MH - Personality Inventory/statistics & numerical data MH - Phenotype MH - Polymorphism, Genetic/*genetics MH - Psychometrics MH - Serotonin Plasma Membrane Transport Proteins/*genetics MH - Social Support EDAT- 2010/02/04 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/02/04 06:00 PHST- 2009/11/14 [received] PHST- 2009/12/22 [revised] PHST- 2009/12/23 [accepted] PHST- 2010/01/31 [aheadofprint] AID - S0165-0327(09)00574-6 [pii] AID - 10.1016/j.jad.2009.12.022 [doi] PST - ppublish SO - J Affect Disord. 2010 Aug;124(3):346-50. Epub 2010 Jan 31. PMID- 20111903 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Associations between XPD polymorphisms and risk of breast cancer: a meta-analysis. PG - 203-12 AB - Studies on polymorphisms of Xeroderma Pigmentosum Group D Protein (XPD) and breast cancer risk are inconclusive. To elucidate the role of XPD genotypes, all available studies were considered in this meta-analysis. The study provided 11,362/10,622 cases/controls for XPD K751Q and 9010/9873 cases/controls for XPD D312N, respectively. Overall, no apparent effects of 751Q allele compared to 751K on breast cancer risk was found in all subjects [RE OR = 1.04, 95% confidence interval (CI) (0.97-1.10), P = 0.28]. Insignificant effects were also found under other genetic contrasts (homologous contrast, dominant model, and recessive model). However, the 751Q allele showed significantly increased risk in Caucasians [FE OR = 1.05, 95% CI (1.00-1.11), P = 0.035]. In addition, insignificant risk effects of D312N polymorphism on breast cancer susceptibility were observed in all subjects under any genetic contrast, but protective effects of 312NN genotype were observed under recessive model [P = 0.02, OR = 0.53, 95% CI (0.32, 0.90)] and homozygote contrast [P = 0.03, OR = 0.55; 95% CI (0.32, 0.96)] in Asians. In summary, our meta-analysis suggested 312N allele might act as a recessive allele in its association with breast cancer and the 751Q allele may play a plausible role in breast cancer development whereas the ethnic background should be carefully concerned in further studies. AD - Department of Colorectal Surgery, Cancer Hospital, Fudan University, Shanghai 200032, China. FAU - Jiang, Zheng AU - Jiang Z FAU - Li, Chunxiang AU - Li C FAU - Xu, Ye AU - Xu Y FAU - Cai, Sanjun AU - Cai S FAU - Wang, Xishan AU - Wang X LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20100129 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 5.99.- (ERCC2 protein, human) RN - EC 5.99.- (Xeroderma Pigmentosum Group D Protein) SB - IM MH - Breast Neoplasms/*genetics MH - Female MH - *Genetic Predisposition to Disease MH - Humans MH - *Polymorphism, Single Nucleotide MH - Risk Factors MH - Xeroderma Pigmentosum Group D Protein/*genetics EDAT- 2010/01/30 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/01/30 06:00 PHST- 2009/11/19 [received] PHST- 2010/01/18 [accepted] PHST- 2010/01/29 [aheadofprint] AID - 10.1007/s10549-010-0751-0 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):203-12. Epub 2010 Jan 29. PMID- 20111902 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Methionine synthase A2756G polymorphism and breast cancer risk: a meta-analysis involving 18,953 subjects. PG - 213-7 AB - The A2756G polymorphism in the methionine synthase (MTR) gene has been implicated in breast cancer risk. However, the published findings are inconsistent. We therefore performed a meta-analysis to investigate this relationship. Eleven published case-control studies, including 8,438 breast cancer cases and 10,515 controls were identified. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the association. Overall, no significant associations between the MTR A2756G polymorphism and breast cancer risk were found for GG versus AA (OR = 0.98, 95% CI: 0.84-1.15), AG versus AA (OR = 0.95, 95% CI: 0.89-1.01), GG/AG versus AA (OR = 0.95, 95% CI = 0.89-1.01), and GG versus AG/AA (OR = 1.00, 95% CI: 0.86-1.17). However, in the stratified analysis, significantly decreased breast cancer risks were found among Europeans (AG versus AA, OR = 0.90, 95% CI = 0.83-0.98; GG/AG versus AA, OR = 0.90, 95% CI = 0.82-0.97) and studies with population-based controls (AG versus AA, OR = 0.93, 95% CI = 0.86-1.00; GG/AG versus AA, OR = 0.93, 95% CI = 0.86-1.00). When stratifying by the menopausal status, no significant result was observed in all genetic models. Taken together, the results suggest that the MTR A2756G polymorphism may contribute to susceptibility to breast cancer among Europeans. AD - Department of Otorhinolaryngology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, People's Republic of China. FAU - Lu, Meiping AU - Lu M FAU - Wang, Feng AU - Wang F FAU - Qiu, Jinrong AU - Qiu J LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20100129 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 2.1.1.13 (5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase) SB - IM MH - 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase/*genetics MH - Breast Neoplasms/*genetics MH - European Continental Ancestry Group/genetics MH - Female MH - *Genetic Predisposition to Disease MH - Humans MH - Polymorphism, Single Nucleotide/*genetics MH - Risk Factors EDAT- 2010/01/30 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/01/30 06:00 PHST- 2010/01/14 [received] PHST- 2010/01/18 [accepted] PHST- 2010/01/29 [aheadofprint] AID - 10.1007/s10549-010-0755-9 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):213-7. Epub 2010 Jan 29. PMID- 20104584 OWN - NLM STAT- MEDLINE DA - 20100226 DCOM- 20101029 IS - 1098-1004 (Electronic) IS - 1059-7794 (Linking) VI - 31 IP - 3 DP - 2010 Mar TI - Characterization of BRCA1 and BRCA2 deleterious mutations and variants of unknown clinical significance in unilateral and bilateral breast cancer: the WECARE study. PG - E1200-40 AB - BRCA1 and BRCA2 screening in women at high-risk of breast cancer results in the identification of both unambiguously defined deleterious mutations and sequence variants of unknown clinical significance (VUS). We examined a population-based sample of young women with contralateral breast cancer (CBC, n=705) or unilateral breast cancer (UBC, n=1398). We identified 470 unique sequence variants, of which 113 were deleterious mutations. The remaining 357 VUS comprised 185 unique missense changes, 60% were observed only once, while 3% occurred with a frequency of >10%. Deleterious mutations occurred three times more often in women with CBC (15.3%) than in women with UBC (5.2%), whereas combined, VUS were observed in similar frequencies in women with CBC and UBC. A protein alignment algorithm defined 16 rare VUS, occurring at highly conserved residues and/or conferring a considerable biochemical difference, the majority located in the BRCA2 DNA-binding domain. We confirm a multiplicity of BRCA1 and BRCA2 VUS that occur at a wide range of allele frequencies. Although some VUS inflict chemical differences at conserved residues, suggesting a deleterious effect, the majority are not associated with an increased risk of CBC. CI - (c) 2010 Wiley-Liss, Inc. AD - Department of Oncology, Clinical Sciences, Lund University, Lund, Sweden. ake.borg@med.lu.se FAU - Borg, Ake AU - Borg A FAU - Haile, Robert W AU - Haile RW FAU - Malone, Kathleen E AU - Malone KE FAU - Capanu, Marinela AU - Capanu M FAU - Diep, Ahn AU - Diep A FAU - Torngren, Therese AU - Torngren T FAU - Teraoka, Sharon AU - Teraoka S FAU - Begg, Colin B AU - Begg CB FAU - Thomas, Duncan C AU - Thomas DC FAU - Concannon, Patrick AU - Concannon P FAU - Mellemkjaer, Lene AU - Mellemkjaer L FAU - Bernstein, Leslie AU - Bernstein L FAU - Tellhed, Lina AU - Tellhed L FAU - Xue, Shanyan AU - Xue S FAU - Olson, Eric R AU - Olson ER FAU - Liang, Xiaolin AU - Liang X FAU - Dolle, Jessica AU - Dolle J FAU - Borresen-Dale, Anne-Lise AU - Borresen-Dale AL FAU - Bernstein, Jonine L AU - Bernstein JL LA - eng GR - CA097397/CA/NCI NIH HHS/United States GR - CA098438/CA/NCI NIH HHS/United States GR - CA131010/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - United States TA - Hum Mutat JT - Human mutation JID - 9215429 RN - 0 (BLID protein, human) RN - 0 (BRCA1 Protein) RN - 0 (BRCA1 protein, human) RN - 0 (BRCA2 Protein) SB - IM MH - Adult MH - Alleles MH - BRCA1 Protein/*genetics MH - BRCA2 Protein/*genetics MH - Breast Neoplasms/*genetics MH - DNA Mutational Analysis MH - Female MH - Gene Deletion MH - Gene Frequency MH - Genetic Variation MH - Humans MH - Middle Aged MH - *Mutation MH - Mutation, Missense MH - Protein Binding PMC - PMC2928257 MID - NIHMS220427 OID - NLM: NIHMS220427 [Available on 03/01/11] OID - NLM: PMC2928257 [Available on 03/01/11] EDAT- 2010/01/28 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/01/28 06:00 PMCR- 2011/03/01 AID - 10.1002/humu.21202 [doi] PST - ppublish SO - Hum Mutat. 2010 Mar;31(3):E1200-40. PMID- 20091231 OWN - NLM STAT- MEDLINE DA - 20100715 DCOM- 20101108 IS - 1557-1920 (Electronic) IS - 1557-1912 (Linking) VI - 12 IP - 4 DP - 2010 Aug TI - Barriers to breast cancer screening among Haitian immigrant women in Little Haiti, Miami. PG - 520-6 AB - Previous research has not examined barriers to mammography screening among Haitian immigrant women through their own discourse. Community Health Workers conducted in-depth interviews with Haitian women in Little Haiti, Miami. We used a grounded theory approach to analyze data from the in-depth interviews. Emergent themes coalesced into three core categories of screening barriers: Structural, Psychosocial, and Socio-Cultural. We developed a model of screening barriers to depict the themes within each core category. Screening barriers must be examined and understood from the social contexts in which they are produced in order to create meaningful interventions. AD - Department of Epidemiology and Public Health, University of Miami Miller School of Medicine, 1120 NW 14th Street, Miami, FL 33136, USA. ekobetz@med.miami.edu FAU - Kobetz, Erin AU - Kobetz E FAU - Menard, Janelle AU - Menard J FAU - Barton, Betsy AU - Barton B FAU - Maldonado, Jennifer Cudris AU - Maldonado JC FAU - Diem, Joshua AU - Diem J FAU - Auguste, Pascale Denize AU - Auguste PD FAU - Pierre, Larry AU - Pierre L LA - eng GR - R21-CA-11981-01/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - J Immigr Minor Health JT - Journal of immigrant and minority health / Center for Minority Public Health JID - 101256527 SB - IM MH - Adult MH - Breast Neoplasms/diagnosis/ethnology/*prevention & control MH - Emigrants and Immigrants MH - Female MH - Florida MH - Haiti/ethnology MH - *Health Services Accessibility MH - Humans MH - Interviews as Topic MH - Mammography/utilization MH - Mass Screening/*utilization MH - Middle Aged EDAT- 2010/01/22 06:00 MHDA- 2010/11/09 06:00 CRDT- 2010/01/22 06:00 AID - 10.1007/s10903-010-9316-x [doi] PST - ppublish SO - J Immigr Minor Health. 2010 Aug;12(4):520-6. PMID- 20087647 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - The association between TA-repeat polymorphism in the promoter region of UGT1A1 and breast cancer risk: a meta-analysis. PG - 879-82 AB - Uridine diphospho-glucuronosyltransferase 1A1 (UGT1A1) plays an important role in breast cancer development. To date, many publications have evaluated the correlation between UGT1A1 TA-repeat polymorphism and breast cancer risk. However, the results remain inconclusive. In order to resolve this conflict, a meta-analysis was performed by searching Medline, PubMed, and ISI Web of Knowledge databases. Seven studies including 5,746 cases and 8,365 controls were collected for UGT1A1 TA-repeat polymorphism. The strength of association between UGT1A1 TA-repeat polymorphism and breast cancer risk was assessed by calculating crude ORs with 95% CIs. Overall, no significant associations between UGT1A1 TA-repeat polymorphism and breast cancer susceptibility were found. In the stratified analysis by ethnicity and source of controls, significant associations were only observed for 6/6 versus 7/7 (OR = 0.88; 95% CI: 0.77-0.99; P = 0.425 for heterogeneity) in Caucasians, but no in other genetic models. In conclusion, this meta-analysis suggests that UGT1A1 A(TA)(7)TAA allele is a potential risk factor for breast cancer in Caucasians. AD - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, People's Republic of China. FAU - Yao, Lei AU - Yao L FAU - Qiu, Li-Xin AU - Qiu LX FAU - Yu, Lu AU - Yu L FAU - Yang, Zhen AU - Yang Z FAU - Yu, Xia-Jia AU - Yu XJ FAU - Zhong, Yang AU - Zhong Y FAU - Yu, Long AU - Yu L LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100120 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 2.4.1.- (bilirubin uridine-diphosphoglucuronosyl transferase 1A1) RN - EC 2.4.1.17 (Glucuronosyltransferase) SB - IM MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - Female MH - *Genetic Predisposition to Disease MH - Glucuronosyltransferase/*genetics MH - Humans MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Risk Factors EDAT- 2010/01/21 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/01/21 06:00 PHST- 2010/01/09 [received] PHST- 2010/01/11 [accepted] PHST- 2010/01/20 [aheadofprint] AID - 10.1007/s10549-010-0742-1 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):879-82. Epub 2010 Jan 20. PMID- 20084546 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - IGFBP3 A-202C polymorphism and breast cancer susceptibility: a meta-analysis involving 33,557 cases and 45,254 controls. PG - 867-71 AB - Published data on the association between insulin-like growth factor binding protein 3 (IGFBP3) A-202C polymorphism and breast cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. Crude ORs with 95% CIs were used to assess the strength of association between them. A total of 27 studies including 33,557 cases and 45,254 controls were involved in this meta-analysis. Overall, significantly elevated breast cancer risk was associated with IGFBP3 C allele when all studies were pooled into the meta-analysis (CC vs. AA: OR = 1.06, 95% CI = 1.02-1.11; dominant model: OR = 1.04, 95% CI = 1.00-1.07). In the subgroup analysis by ethnicity, significantly increased risk was found for Caucasians (AC vs. AA: OR = 1.04, 95% CI = 1.00-1.08; CC vs. AA: OR = 1.05, 95% CI = 1.01-1.10; dominant model: OR = 1.04, 95% CI = 1.00-1.08) and Asians (CC vs. AA: OR = 1.35, 95% CI = 1.02-1.78; recessive model: OR = 1.38, 95% CI = 1.05-1.82). When stratified by study design, statistically significantly elevated risk was found among population-based studies (CC vs. AA: OR = 1.06, 95% CI = 1.01-1.11; dominant model: OR = 1.03, 95% CI = 1.00-1.07). In the subgroup analysis by menopausal status, no statistically significantly increased risk was found among premenopausal or postmenopausal women. In conclusion, this meta-analysis suggests that the IGFBP3 C allele is a low-penetrant risk factor for developing breast cancer. AD - Department of Medical Oncology, Cancer Hospital, Fudan University, Shanghai, China. FAU - Qiu, Li-Xin AU - Qiu LX FAU - Yao, Lei AU - Yao L FAU - Yuan, Hui AU - Yuan H FAU - Mao, Chen AU - Mao C FAU - Chen, Bo AU - Chen B FAU - Zhan, Ping AU - Zhan P FAU - Xue, Kai AU - Xue K FAU - Zhang, Jian AU - Zhang J FAU - Hu, Xi-Chun AU - Hu XC LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20100119 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (IGFBP3 protein, human) RN - 0 (Insulin-Like Growth Factor Binding Proteins) SB - IM MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - Female MH - *Genetic Predisposition to Disease MH - Humans MH - Insulin-Like Growth Factor Binding Proteins/*genetics MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Risk Factors EDAT- 2010/01/20 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/01/20 06:00 PHST- 2010/01/06 [received] PHST- 2010/01/08 [accepted] PHST- 2010/01/19 [aheadofprint] AID - 10.1007/s10549-010-0739-9 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):867-71. Epub 2010 Jan 19. PMID- 20080807 OWN - NLM STAT- MEDLINE DA - 20100720 DCOM- 20101101 IS - 1465-3648 (Electronic) IS - 0268-1153 (Linking) VI - 25 IP - 4 DP - 2010 Aug TI - Young women's responses to smoking and breast cancer risk information. PG - 668-77 AB - Current evidence confirms that young women who smoke or who have regular long-term exposure to secondhand smoke (SHS) have an increased risk of developing premenopausal breast cancer. The aim of this research was to examine the responses of young women to health information about the links between active smoking and SHS exposure and breast cancer and obtain their advice about messaging approaches. Data were collected in focus groups with 46 women, divided in three age cohorts: 15-17, 18-19 and 20-24 and organized according to smoking status (smoking, non-smoking and mixed smoking status groups). The discussion questions were preceded by information about passive and active smoking and its associated breast cancer risk. The study findings show young women's interest in this risk factor for breast cancer. Three themes were drawn from the analysis: making sense of the information on smoking and breast cancer, personal susceptibility and tobacco exposure and suggestions for increasing awareness about tobacco exposure and breast cancer. There was general consensus on framing public awareness messages about this risk factor on 'protecting others' from breast cancer to catch smokers' attention, providing young women with the facts and personal stories of breast cancer to help establish a personal connection with this information and overcome desensitization related to tobacco messages, and targeting all smokers who may place young women at risk. Cautions were also raised about the potential for stigmatization. Implications for raising awareness about this modifiable risk factor for breast cancer are discussed. AD - Institute for Healthy Living.hronic Disease Prevention, University of British Columbia Okanagan, Kelowna, BC, Canada. Joan.bottorff@ubc.ca FAU - Bottorff, Joan L AU - Bottorff JL FAU - McKeown, Stephanie Barclay AU - McKeown SB FAU - Carey, Joanne AU - Carey J FAU - Haines, Rebecca AU - Haines R FAU - Okoli, Chizimuzo AU - Okoli C FAU - Johnson, Kenneth C AU - Johnson KC FAU - Easley, Julie AU - Easley J FAU - Ferrence, Roberta AU - Ferrence R FAU - Baillie, Lynne AU - Baillie L FAU - Ptolemy, Erin AU - Ptolemy E LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100115 PL - England TA - Health Educ Res JT - Health education research JID - 8608459 RN - 0 (Tobacco Smoke Pollution) SB - T MH - Adolescent MH - Adult MH - Awareness MH - Breast Neoplasms/*etiology MH - Female MH - Focus Groups MH - Health Education/organization & administration MH - Humans MH - Prejudice MH - Risk Factors MH - Smoking/*adverse effects MH - Tobacco Smoke Pollution/*adverse effects MH - Young Adult PMC - PMC2905920 OID - NLM: PMC2905920 EDAT- 2010/01/19 06:00 MHDA- 2010/11/03 06:00 CRDT- 2010/01/19 06:00 PHST- 2010/01/15 [aheadofprint] AID - cyp067 [pii] AID - 10.1093/her/cyp067 [doi] PST - ppublish SO - Health Educ Res. 2010 Aug;25(4):668-77. Epub 2010 Jan 15. PMID- 20077502 OWN - NLM STAT- MEDLINE DA - 20100226 DCOM- 20101029 IS - 1098-1004 (Electronic) IS - 1059-7794 (Linking) VI - 31 IP - 3 DP - 2010 Mar TI - Cancer predisposing missense and protein truncating BARD1 mutations in non-BRCA1 or BRCA2 breast cancer families. PG - E1175-85 AB - Fifteen years ago BRCA1 and BRCA2 were reported as high penetrant breast cancer predisposing genes. However, mutations in these genes are found in only a fraction of high risk families. BARD1 is a candidate breast cancer gene, but only a limited number of missense mutations with rather unclear pathogenic consequences have been reported.We screened 196 high risk breast cancer families for the occurrence of BARD1 variants. All genetic variants were analyzed using clinical information as well as IN SILICO predictive tools, including protein modeling. We found three candidate pathogenic mutations in seven families including a first case of a protein truncating mutation (p.Glu652fs) removing the entire second BRCT domain of BARD1. In conclusion, we provide evidence for an increased breast cancer risk associated to specific BARD1 germline mutations. However, these BARD1 mutations occur in a minority of hereditary breast cancer families. CI - (c)2010 Wiley-Liss, Inc. AD - Laboratory of Molecular Oncology, Vrije Universiteit Brussel, 1090 Brussels, Belgium. FAU - De Brakeleer, Sylvia AU - De Brakeleer S FAU - De Greve, Jacques AU - De Greve J FAU - Loris, Remy AU - Loris R FAU - Janin, Nicolas AU - Janin N FAU - Lissens, Willy AU - Lissens W FAU - Sermijn, Erica AU - Sermijn E FAU - Teugels, Erik AU - Teugels E LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Hum Mutat JT - Human mutation JID - 9215429 RN - 0 (BARD1 protein, human) RN - 0 (Tumor Suppressor Proteins) RN - EC 6.3.2.19 (Ubiquitin-Protein Ligases) SB - IM MH - Breast Neoplasms/*genetics MH - Computational Biology/methods MH - Family Health MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - *Genetic Predisposition to Disease MH - Genetic Variation MH - Humans MH - Male MH - *Mutation MH - *Mutation, Missense MH - Ovarian Neoplasms/genetics MH - Pedigree MH - Tumor Suppressor Proteins/*genetics MH - Ubiquitin-Protein Ligases/*genetics EDAT- 2010/01/16 06:00 MHDA- 2010/10/30 06:00 CRDT- 2010/01/16 06:00 AID - 10.1002/humu.21200 [doi] PST - ppublish SO - Hum Mutat. 2010 Mar;31(3):E1175-85. PMID- 20076999 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - No association between a progesterone receptor gene promoter polymorphism (+331G>A) and breast cancer risk in Caucasian women: evidence from a literature-based meta-analysis. PG - 853-8 AB - Sex steroid hormones and their receptors such as estrogen receptor (ER) and progesterone receptor (PgR) have been widely studied for their roles in the etiology of breast cancer. To date, many studies have evaluated the association between a functional polymorphism in the PgR gene promoter (+331G>A, rs10895068) and breast cancer risk; however, the result is still ambiguous and inconclusive. In order to derive a more precise estimation of the association, a meta-analysis was performed in this study. By searching relevant literature, a total of 10 studies containing 13,702 cases and 14,726 controls (28,428 subjects in total) were identified and meta-analyzed. All the study subjects were Caucasian women. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association in the codominant model, dominant model, and recessive model. Overall, no significant association between +331G>A polymorphism and breast cancer susceptibility was observed for AA versus GG (OR = 0.940, 95% CI: 0.566-1.562), GA versus GG (OR = 1.061, 95% CI: 0.888-1.267), AA + GA versus GG (OR = 1.074, 95% CI: 0.956-1.207), and AA versus GA + GG (OR = 0.951, 95% CI: 0.586-1.544). Sensitivity analysis was performed by limiting the meta-analysis to those studies fulfilling Hardy-Weinberg equilibrium, and the results were not materially altered in any genetic model. In conclusion, the present meta-analysis strongly suggests that +331G>A in the PgR gene is not associated with breast cancer risk. AD - Department of Breast Surgery, Cancer Hospital/Cancer Institute, Fudan University, 399 Ling-Ling Road, 200032 Shanghai, People's Republic of China. FAU - Yu, Ke-Da AU - Yu KD FAU - Chen, Ao-Xiang AU - Chen AX FAU - Shao, Zhi-Ming AU - Shao ZM LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20100114 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Receptors, Progesterone) SB - IM MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - Female MH - *Genetic Predisposition to Disease MH - Humans MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Receptors, Progesterone/*genetics MH - Risk Factors EDAT- 2010/01/16 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/01/16 06:00 PHST- 2010/01/05 [received] PHST- 2010/01/07 [accepted] PHST- 2010/01/14 [aheadofprint] AID - 10.1007/s10549-010-0738-x [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):853-8. Epub 2010 Jan 14. PMID- 20058067 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - The hOGG1 Ser326Cys polymorphism and breast cancer risk: a meta-analysis. PG - 835-42 AB - It was reported that the functional polymorphism Ser326Cys in the human 8-oxoguanine DNA glycosylase gene was associated with breast cancer risk; however, the published studies have inconsistent conclusions. To elucidate the effect of hOGG1 Ser326Cys on the susceptibility to breast cancer, all available studies were collected in this meta-analysis. We extracted the data from 10 case-control studies that were published in the PubMed database from 2003 to 2008 using the search phrases "human 8-oxoguanine DNA glycosylase, hOGG1, OGG1, OGG, polymorphism, genetic variation, and breast cancer." This meta-analysis included 4,963 breast cancer cases and 4,776 control subjects. The results showed that individuals who carrying the hOGG1 326Cys allele in the additive model did not have significantly increased risk of breast cancer compared with those carrying the 326Ser allele (P = 0.47, OR = 1.02; 95% CI = 0.96-1.09); similarly, no significant association between the hOGG1 326Cys allele and breast cancer risk was found either in the recessive genetic model (P = 0.34, OR = 1.06; 95% CI = 0.94-1.18) for Cys/Cys versus Ser/Cys + Ser/Ser, or dominant genetic model (P = 0.78, OR = 1.01; 95% CI = 0.93-1.11) for Cys/Cys + Ser/Cys versus Ser/Ser. In the stratified analysis, the meta-analysis showed the association between hOGG1 326Cys allele in the additive model and breast cancer was significant in European subjects (P = 0.04, OR = 0.71; 95% CI = 0.51-0.98), and dominant genetic model (P = 0.004, OR = 0.44; 95% CI = 0.25-0.77). However, the association was not significant between this polymorphism and different menopausal status (premenopausal and postmenopausal) and the other ethnicities (Asians and Americans). The meta-analysis suggested that the hOGG1 326Cys allele plays a significant protective effect to breast cancer in European women. AD - Institute of Cancer Prevention and Treatment, Harbin Medical University, Baojian Road 6, Nangang District, 150081 Harbin, China. FAU - Yuan, Weiguang AU - Yuan W FAU - Xu, Lidan AU - Xu L FAU - Feng, Yuanxi AU - Feng Y FAU - Yang, Yue AU - Yang Y FAU - Chen, Wangyang AU - Chen W FAU - Wang, Jingwei AU - Wang J FAU - Pang, Da AU - Pang D FAU - Li, Dianjun AU - Li D LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20100108 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 3.2.2.- (DNA Glycosylases) RN - EC 3.2.2.- (oxoguanine glycosylase 1, human) SB - IM MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - DNA Glycosylases/*genetics MH - Female MH - *Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Risk Factors EDAT- 2010/01/09 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/01/09 06:00 PHST- 2009/10/31 [received] PHST- 2009/12/24 [accepted] PHST- 2010/01/08 [aheadofprint] AID - 10.1007/s10549-009-0722-5 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):835-42. Epub 2010 Jan 8. PMID- 20054644 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - Variants in DNA double-strand break repair genes and risk of familial breast cancer in a South American population. PG - 813-22 AB - The double-strand break (DSB) DNA repair pathway has been implicated in breast cancer (BC). RAD51 and its paralogs XRCC3 and RAD51D play an important role in the repair of DSB through homologous recombination (HR). Some polymorphisms including XRCC3-Thr241Met, RAD51-135G>C, and RAD51D-E233G have been found to confer increased BC susceptibility. In order to detect novel mutations that may contribute to BC susceptibility, 150 patients belonging to 150 Chilean BRCA1/2-negative families were screened for mutations in XRCC3. No mutations were detected in the XRCC3 gene. In addition, using a case-control design we studied the XRCC3-Thr241Met, and RAD51D-E233G polymorphisms in 267 BC cases and 500 controls to evaluate their possible association with BC susceptibility. The XRCC3 Met/Met genotype was associated with an increased BC risk (P = 0.003, OR = 2.44 [95%CI 1.34-4.43]). We did not find an association between E233G polymorphism and BC risk. We also analyzed the effect of combined genotypes among RAD51-135G>C, Thr241Met, and E233G polymorphisms on BC risk. No interaction was observed between Thr241Met and 135G>C. The combined genotype Thr/Met-E/G was associated with an increased BC risk among women who (a) have a family history of BC, (b) are BRCA1/2-negative, and (c) were <50 years at onset (n = 195) (P = 0.037, OR = 10.5 [95%CI 1.16-94.5]). Our results suggested that the variability of the DNA HR repair genes XRCC3 and RAD51D may play a role in BC risk, but this role may be underlined by a mutual interaction between these genes. These findings should be confirmed in other populations. AD - Human Genetics Program, Institute of Biomedical Sciences (ICBM), School of Medicine, University of Chile, Av. Independencia 1027, P.O. Box 70061, Santiago, Chile. ljara@med.uchile.cl FAU - Jara, Lilian AU - Jara L FAU - Dubois, Karen AU - Dubois K FAU - Gaete, Daniel AU - Gaete D FAU - de Mayo, Tomas AU - de Mayo T FAU - Ratkevicius, Nikalai AU - Ratkevicius N FAU - Bravo, Teresa AU - Bravo T FAU - Margarit, Sonia AU - Margarit S FAU - Blanco, Rafael AU - Blanco R FAU - Gomez, Fernando AU - Gomez F FAU - Waugh, Enrique AU - Waugh E FAU - Peralta, Octavio AU - Peralta O FAU - Reyes, Jose M AU - Reyes JM FAU - Ibanez, Gladys AU - Ibanez G FAU - Gonzalez-Hormazabal, Patricio AU - Gonzalez-Hormazabal P LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100107 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (DNA-Binding Proteins) RN - 0 (RAD51L3 protein, human) RN - 0 (X-ray repair cross complementing protein 3) SB - IM MH - Adult MH - Aged MH - Breast Neoplasms/epidemiology/*genetics MH - Case-Control Studies MH - *DNA Breaks, Double-Stranded MH - DNA Mutational Analysis MH - DNA Repair/*genetics MH - DNA-Binding Proteins/*genetics MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Middle Aged MH - Polymorphism, Genetic/*genetics MH - Prognosis MH - Risk Factors MH - South America/epidemiology EDAT- 2010/01/08 06:00 MHDA- 2010/10/27 06:00 CRDT- 2010/01/08 06:00 PHST- 2009/10/14 [received] PHST- 2009/12/21 [accepted] PHST- 2010/01/07 [aheadofprint] AID - 10.1007/s10549-009-0709-2 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):813-22. Epub 2010 Jan 7. PMID- 20054640 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Concordance of HER2 in primary tumor and leptomeningeal metastases: now what? PG - 129-31 AD - Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA. nlin@partners.org FAU - Lin, Nancy U AU - Lin NU LA - eng PT - Comment PT - Journal Article DEP - 20100107 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CON - Breast Cancer Res Treat. 2010 Aug;123(1):125-8. PMID: 19916047 MH - Breast Neoplasms/cerebrospinal fluid/*genetics/*secondary MH - Cerebrospinal Fluid/cytology MH - Female MH - *Genes, erbB-2 MH - Humans MH - Meningeal Carcinomatosis/cerebrospinal fluid/*genetics/*secondary MH - Receptor, erbB-2/genetics EDAT- 2010/01/08 06:00 MHDA- 2010/11/10 06:00 CRDT- 2010/01/08 06:00 PHST- 2009/12/08 [received] PHST- 2009/12/24 [accepted] PHST- 2010/01/07 [aheadofprint] AID - 10.1007/s10549-009-0720-7 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):129-31. Epub 2010 Jan 7. PMID- 20037779 OWN - NLM STAT- MEDLINE DA - 20100720 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Molecular predictors of efficacy of adjuvant weekly paclitaxel in early breast cancer. PG - 149-57 AB - Treatment with fluororacil, epirubicin, and cyclophosphamide followed by weekly paclitaxel (FEC-P) yielded superior disease-free survival than FEC in the adjuvant breast cancer trial GEICAM 9906. We evaluate molecular subtypes predictive of prognosis and paclitaxel response in this trial. Two molecular subtype classifications based on conventional immunohistochemical and fluorescent in situ hybridization determinations were used: #1: Four groups segregated according to the combination of hormone receptor (HR) and HER2 status; #2: Intrinsic subtype classification (Triple Negative (TN), HER2, Luminal B and Luminal A). Results: Both subtype classifications yielded prognostic and predictive information. HR +/HER2- patients (and Luminal A patients) had a significantly better outcome than the other subgroups of patients. The superiority of FEC-P over FEC was clearly more marked in HR-/HER2- patients (TN patients), particularly in the subset with basal phenotype (TN and either EGFR+ or cytokeratins 5/6+). The Luminal A subtype also achieved a significant benefit with FEC-P. The molecular-defined subgroup of TN was clearly predictive of better response to treatment with FEC-P. Luminal A patients had the best prognosis and also have a better outcome with weekly paclitaxel. AD - Servicio de Oncologia Medica, Departmento de Oncologia, Hospital General Universitario Gregorio Maranon, 28009 Madrid, Spain. mmartin@geicam.org FAU - Martin, Miguel AU - Martin M FAU - Rodriguez-Lescure, Alvaro AU - Rodriguez-Lescure A FAU - Ruiz, Amparo AU - Ruiz A FAU - Alba, Emilio AU - Alba E FAU - Calvo, Lourdes AU - Calvo L FAU - Ruiz-Borrego, Manuel AU - Ruiz-Borrego M FAU - Santaballa, Ana AU - Santaballa A FAU - Rodriguez, Cesar A AU - Rodriguez CA FAU - Crespo, Carmen AU - Crespo C FAU - Abad, Mar AU - Abad M FAU - Dominguez, Severina AU - Dominguez S FAU - Florian, Jesus AU - Florian J FAU - Llorca, Cristina AU - Llorca C FAU - Mendez, Miguel AU - Mendez M FAU - Godes, Maria AU - Godes M FAU - Cubedo, Ricardo AU - Cubedo R FAU - Murias, Adolfo AU - Murias A FAU - Batista, Norberto AU - Batista N FAU - Garcia, Maria Jose AU - Garcia MJ FAU - Caballero, Rosalia AU - Caballero R FAU - de Alava, Enrique AU - de Alava E LA - eng PT - Clinical Trial, Phase III PT - Journal Article PT - Multicenter Study PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Antineoplastic Agents) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Markers, Biological) RN - 33069-62-4 (Paclitaxel) RN - 50-18-0 (Cyclophosphamide) RN - 51-21-8 (Fluorouracil) RN - 56420-45-2 (Epirubicin) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - Antineoplastic Agents/*therapeutic use MH - Antineoplastic Combined Chemotherapy Protocols/therapeutic use MH - Breast Neoplasms/classification/*drug therapy/*genetics MH - Chemotherapy, Adjuvant MH - Cyclophosphamide/administration & dosage MH - Disease-Free Survival MH - Epirubicin/administration & dosage MH - Female MH - Fluorouracil/administration & dosage MH - Humans MH - Immunohistochemistry MH - In Situ Hybridization, Fluorescence MH - Kaplan-Meiers Estimate MH - Paclitaxel/*therapeutic use MH - Prognosis MH - Receptor, erbB-2/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics MH - Treatment Outcome MH - Tumor Markers, Biological/*analysis EDAT- 2009/12/29 06:00 MHDA- 2010/11/10 06:00 CRDT- 2009/12/29 06:00 PHST- 2009/08/25 [received] PHST- 2009/11/21 [accepted] PHST- 2009/12/27 [aheadofprint] AID - 10.1007/s10549-009-0663-z [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):149-57. PMID- 20035378 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - TNFalpha -308 G/A polymorphism is associated with breast cancer risk: a meta-analysis involving 10,184 cases and 12,911 controls. PG - 267-71 AB - Tumor necrosis factor alpha (TNFalpha) is a pleiotropic cytokine which can regulate a wide variety of cellular responses. Low concentrations of TNFalpha seem to increase tumor growth and progression. The -308 G/A polymorphism in TNFalpha has been implicated in breast cancer risk but the published data remain inconclusive. In order to derive a more precise estimation of the relationship, a meta-analysis was performed by searching PubMed, Web of Science, ScienceDirect, EBSCO, CNKI, and Chinese Biomedicine Database. 11 studies including 10,184 cases and 12,911 controls were collected for TNFalpha -308 G/A polymorphism. Crude ORs with 95% CIs were used to assess the strength of association between the TNFalpha -308 G/A polymorphism and breast cancer risk. The pooled ORs were performed for codominant model (GG versus AA; GA versus AA), dominant model (GG + GA versus AA), recessive model (GG versus GA + AA), and G allele versus A allele, respectively. Overall, significantly elevated breast cancer risk was found for recessive model (OR = 1.10, 95% CI = 1.04-1.17) and for G allele versus A allele (OR = 1.08, 95% CI = 1.02-1.14). In the subgroup analysis by ethnicity, significantly increased risks were also found among Caucasians for recessive model and for G allele versus A allele (for recessive model: OR = 1.10, 95% CI = 1.04-1.17; for G allele versus A allele: OR = 1.09, 95% CI = 1.03-1.14). However, no significant associations were found among Asians for all genetic models. In conclusion, this meta-analysis suggests that the TNFalpha -308 G allele is a risk factor for developing breast cancer, especially for Caucasians. AD - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China. FAU - Fang, Fang AU - Fang F FAU - Yao, Lei AU - Yao L FAU - Yu, Xiao Jia AU - Yu XJ FAU - Yu, Lu AU - Yu L FAU - Wu, Qi AU - Wu Q FAU - Yu, Long AU - Yu L LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20091225 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Alleles MH - Asian Continental Ancestry Group/genetics/statistics & numerical data MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Ethnic Groups/genetics/statistics & numerical data MH - European Continental Ancestry Group/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Menopause MH - Models, Genetic MH - Odds Ratio MH - *Polymorphism, Single Nucleotide MH - Risk MH - Risk Factors MH - Tumor Necrosis Factor-alpha/*genetics EDAT- 2009/12/26 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/26 06:00 PHST- 2009/12/14 [received] PHST- 2009/12/16 [accepted] PHST- 2009/12/25 [aheadofprint] AID - 10.1007/s10549-009-0698-1 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):267-71. Epub 2009 Dec 25. PMID- 20033770 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - The functional promoter polymorphism (-842G>C) in the PIN1 gene is associated with decreased risk of breast cancer in non-Hispanic white women 55 years and younger. PG - 243-9 AB - PIN1, an isomerase that causes conformational changes in proteins, plays an important role in mammary epithelial cell growth both physiologically and pathologically. Thus, genetic variants in the PIN1 gene may alter protein function and cancer risk. We have previously demonstrated an association between a PIN1 promoter variant (-842G>C; rs2233678) and risk of squamous cell carcinoma of the head and neck, a finding supported by additional functional data. In the present study, we genotyped two promoter single nucleotide polymorphisms (SNPs) (-842G>C, rs2233678 and -667T>C, rs2233679) and one synonymous SNP (Gln33Gln; G>A, rs2233682) in exon 2 to evaluate their associations with risk of sporadic breast cancer in non-Hispanic white women 55 years and younger. We found that the carriers of -842C variant alleles had decreased risk of breast cancer with an adjusted odd ratio (OR) of 0.67 and 95% confidence interval (CI) of 0.50-0.90. This reduced risk was more evident in women after reproductive age of 45 (OR = 0.63, 95% CI = 0.42-0.93), ever-smokers (OR = 0.56, 95% CI = 0.36-0.88), and ever-drinkers (OR = 0.67, 95% CI = 0.45-0.99). No such associations were observed for PIN1 -667T>C and PIN1 Gln33Gln. However, the haplotypes of these three SNPs were also associated with reduced risk of breast cancer. In conclusion, the PIN1 polymorphisms may contribute to the etiology of sporadic breast cancer in non-Hispanic white women 55 years and younger. Further validation in large population-based studies is needed. AD - Department of Epidemiology, Unit 1365, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA. FAU - Han, Chan H AU - Han CH FAU - Lu, Jiachun AU - Lu J FAU - Wei, Qingyi AU - Wei Q FAU - Bondy, Melissa L AU - Bondy ML FAU - Brewster, Abenaa M AU - Brewster AM FAU - Yu, Tse-Kuan AU - Yu TK FAU - Buchholz, Thomas A AU - Buchholz TA FAU - Arun, Banu K AU - Arun BK FAU - Wang, Li-E AU - Wang LE LA - eng GR - P30 CA016672/CA/NCI NIH HHS/United States GR - P50 CA116199/CA/NCI NIH HHS/United States GR - R01 CA131274/CA/NCI NIH HHS/United States GR - R01 ES011740/ES/NIEHS NIH HHS/United States GR - R03 CA108364/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20091224 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (NIMA-interacting peptidylprolyl isomerase) RN - EC 5.2.1.8 (Peptidylprolyl Isomerase) SB - IM MH - Adult MH - Age Factors MH - Aged MH - Alcohol Drinking/epidemiology MH - Breast Neoplasms/*epidemiology/genetics MH - Carcinoma/*epidemiology/genetics MH - Case-Control Studies MH - Ethnic Groups/genetics/statistics & numerical data MH - European Continental Ancestry Group/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Haplotypes MH - Humans MH - Middle Aged MH - Peptidylprolyl Isomerase/*genetics MH - *Polymorphism, Genetic MH - Polymorphism, Single Nucleotide/*genetics MH - Risk MH - Smoking/epidemiology PMC - PMC2883663 MID - NIHMS194195 OID - NLM: NIHMS194195 [Available on 07/01/11] OID - NLM: PMC2883663 [Available on 07/01/11] EDAT- 2009/12/25 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/25 06:00 PMCR- 2011/07/01 PHST- 2009/12/07 [received] PHST- 2009/12/08 [accepted] PHST- 2009/12/24 [aheadofprint] AID - 10.1007/s10549-009-0682-9 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):243-9. Epub 2009 Dec 24. PMID- 20033767 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Current evidence on the relationship between polymorphisms in the COX-2 gene and breast cancer risk: a meta-analysis. PG - 251-7 AB - The association between single-nucleotide polymorphisms (SNPs) in the COX-2 gene and breast cancer risk is still ambiguous. We here try to derive a more precise estimation of the relationship by performing a meta-analysis based on currently available evidence from literature. More than 15 SNPs have been studied, and the most studied genetic variants were rs5275, rs5277, and rs20417. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association between each polymorphism and breast cancer risk under the codominant model, dominant model, and recessive model, respectively (nine studies with 6,968 cases and 9,126 controls for rs5275; three studies with 2,901 cases and 3,463 controls for rs20417; two studies with 5,551 cases and 6,208 controls for rs5277). No overall significant associations were observed in single-locus analysis between the three polymorphisms of COX-2 and breast cancer risk, though a borderline significant increased risk of breast cancer was detected with rs5277 in a recessive model (OR: 1.217, 95% CI: 0.958-1.547, P = 0.107). The results were not changed when studies were stratified by ethnicity. In conclusion, the present meta-analysis suggests that none of the most studied three SNPs (rs5275, rs20417, and rs5277) in the COX-2 gene is a conspicuous low-penetrant risk factor for developing breast cancer. There is a need for further large studies into the role of these polymorphisms (especially rs5277) and other potentially functional polymorphisms/haplotypes in the COX-2 gene as breast cancer risk modifiers. AD - Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China. FAU - Yu, Ke-Da AU - Yu KD FAU - Chen, Ao-Xiang AU - Chen AX FAU - Yang, Chen AU - Yang C FAU - Qiu, Li-Xin AU - Qiu LX FAU - Fan, Lei AU - Fan L FAU - Xu, Wen-Huan AU - Xu WH FAU - Shao, Zhi-Ming AU - Shao ZM LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20091224 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 1.14.99.1 (Cyclooxygenase 2) RN - EC 1.14.99.1 (PTGS2 protein, human) SB - IM MH - Breast Neoplasms/*epidemiology/genetics MH - Case-Control Studies MH - Cohort Studies MH - Cyclooxygenase 2/*genetics MH - Ethnic Groups/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Models, Genetic MH - Odds Ratio MH - Penetrance MH - *Polymorphism, Single Nucleotide MH - Prospective Studies MH - Retrospective Studies MH - Risk EDAT- 2009/12/25 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/25 06:00 PHST- 2009/12/09 [received] PHST- 2009/12/11 [accepted] PHST- 2009/12/24 [aheadofprint] AID - 10.1007/s10549-009-0688-3 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):251-7. Epub 2009 Dec 24. PMID- 20033766 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Lack of association between CYP17 MspA1 polymorphism and breast cancer risk: a meta-analysis of 22,090 cases and 28,498 controls. PG - 259-65 AB - Epidemiological studies have evaluated the association between CYP17 MspA1 polymorphism and breast cancer risk. However, the results remain conflicting rather than conclusive. To derive a more precise estimation of the relationship, we performed this meta-analysis. Systematic searches of the PubMed and Medline databases were performed. A total of 35 studies including 22,090 cases and 28,498 controls were identified. Genotype distributions of CYP17 in the controls of all studies were in agreement with Hardy-Weinberg equilibrium (HWE) except for three studies. When all 35 studies were pooled into the meta-analysis, there was no evidence for significant association between CYP17 MspA1 polymorphism and breast cancer risk (for A1/A2 vs. A1/A1: OR = 1.00, 95% CI = 0.96-1.04; for A2/A2 vs. A1/A1: OR = 1.03, 95% CI = 0.97-1.08; for dominant model: OR = 1.01, 95% CI = 0.97-1.05; for recessive model: OR = 1.03, 95% CI = 0.98-1.08). In the subgroup analyses by ethnicity, menopausal status and source of controls, no significant associations were found in all genetic models. When sensitivity analyses were performed by excluding HWE-violating studies, all the results were not materially altered. In summary, the meta-analysis strongly suggests that CYP17 MspA1 polymorphism is not associated with increased breast cancer risk. AD - Department of Epidemiology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, China. FAU - Mao, Chen AU - Mao C FAU - Wang, Xi-Wen AU - Wang XW FAU - He, Ben-Fu AU - He BF FAU - Qiu, Li-Xin AU - Qiu LX FAU - Liao, Ru-Yan AU - Liao RY FAU - Luo, Rong-Cheng AU - Luo RC FAU - Chen, Qing AU - Chen Q LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20091224 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 1.14.99.9 (CYP17A1 protein, human) RN - EC 1.14.99.9 (Steroid 17-alpha-Hydroxylase) SB - IM MH - Amino Acid Substitution MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Ethnic Groups/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Menopause MH - Models, Genetic MH - Odds Ratio MH - Patient Selection MH - *Polymorphism, Restriction Fragment Length MH - *Polymorphism, Single Nucleotide MH - Risk MH - Steroid 17-alpha-Hydroxylase/*genetics EDAT- 2009/12/25 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/25 06:00 PHST- 2009/12/12 [received] PHST- 2009/12/14 [accepted] PHST- 2009/12/24 [aheadofprint] AID - 10.1007/s10549-009-0695-4 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):259-65. Epub 2009 Dec 24. PMID- 20033481 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - No association between CYP1B1 Val432Leu polymorphism and breast cancer risk: a meta-analysis involving 40,303 subjects. PG - 237-42 AB - Breast cancer is the most common cancer in women. To date, many publications have evaluated the association between Cytochrome P450 1B1 (CYP1B1) Val432Leu polymorphism and breast cancer risk. However, the results remain inconclusive. In order to derive a more precise estimation of the association, a meta-analysis was performed in this study. By searching Medline, Pubmed, and ISI Web of Knowledge databases, 26 studies including 19,028 cases and 21,275 controls were collected for CYP1B1 Val432Leu polymorphism. Crude ORs with 95% CIs were used to assess the strength of association between CYP1B1 Val432Leu polymorphism and breast cancer risk. The pooled ORs were performed for codominant model, dominant model, and recessive model, respectively. Overall, no significant associations between CYP1B1 Val432Leu polymorphism and breast cancer susceptibility were found for Val/Val versus Leu/Leu (OR = 0.98; 95% CI: 0.90-1.06), Val/Leu versus Leu/Leu (OR = 1.01; 95% CI: 0.93-1.09), Val/Val + Val/Leu versus Leu/Leu (OR = 1.00; 95% CI: 0.93-1.08) and Val/Val versus Val/Leu + Leu/Leu (OR = 0.96; 95% CI: 0.91-1.01). In the stratified analysis by ethnicity, menopausal status and sources of controls, significant associations were still not observed in all genetic models. In conclusion, this meta-analysis provides strong evidence that CYP1B1 Val432Leu polymorphism is not associated with breast cancer risk. AD - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, 200433 Shanghai, People's Republic of China. FAU - Yao, Lei AU - Yao L FAU - Fang, Fang AU - Fang F FAU - Wu, Qi AU - Wu Q FAU - Zhong, Yang AU - Zhong Y FAU - Yu, Long AU - Yu L LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20091224 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (CYP1B1 protein, human) RN - 9035-51-2 (Cytochrome P-450 Enzyme System) SB - IM CIN - Breast Cancer Res Treat. 2010 Nov;124(1):293-4. PMID: 20686834 MH - Amino Acid Substitution MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Cytochrome P-450 Enzyme System/*genetics MH - Ethnic Groups/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Menopause MH - Odds Ratio MH - *Polymorphism, Single Nucleotide MH - Risk EDAT- 2009/12/25 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/25 06:00 PHST- 2009/12/10 [received] PHST- 2009/12/12 [accepted] PHST- 2009/12/24 [aheadofprint] AID - 10.1007/s10549-009-0689-2 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):237-42. Epub 2009 Dec 24. PMID- 20013047 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - No association between CYP17 T-34C polymorphism and breast cancer risk: a meta-analysis involving 58,814 subjects. PG - 221-7 AB - Breast cancer is one of the most common malignant tumors worldwide. To date, many articles have evaluated the association between Cytochrome P450c17 (CYP17) T-34C polymorphism and breast cancer risk. However, the results remain inconclusive. In order to derive a more precise estimation of the association, a meta-analysis was performed in this study. By searching Medline, ISI Web of Knowledge, Cochrane, ScienceDirect, EBSCO, CNKI, and SinoMed databases, 43 studies including 26,008 cases and 32,806 controls were collected for CYP17 T-34C polymorphism. Crude ORs with 95% CIs were used to assess the strength of association between CYP17 T-34C polymorphism and breast cancer risk. The pooled ORs were performed for codominant model, dominant model, and recessive model, respectively. Overall, no significant associations between CYP17 T-34C polymorphism and breast cancer susceptibility were found for TT versus CC (OR = 0.96; 95% CI: 0.89-1.05), TC versus CC (OR = 0.97; 95% CI: 0.89-1.06), TT + TC versus CC (OR = 0.97; 95% CI: 0.89-1.05) and TT versus TC + CC (OR = 0.98; 95% CI: 0.93-1.03). In the stratified analysis by ethnicity, menopausal status, and sources of controls, significant associations were still not detected in all genetic models. In conclusion, this meta-analysis strongly suggests that CYP17 T-34C polymorphism is not associated with breast cancer risk. AD - State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, 200433 Shanghai, People's Republic of China. FAU - Yao, Lei AU - Yao L FAU - Fang, Fang AU - Fang F FAU - Wu, Qi AU - Wu Q FAU - Yang, Zhen AU - Yang Z FAU - Zhong, Yang AU - Zhong Y FAU - Yu, Long AU - Yu L LA - eng PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't DEP - 20091215 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (5' Untranslated Regions) RN - EC 1.14.99.9 (CYP17A1 protein, human) RN - EC 1.14.99.9 (Steroid 17-alpha-Hydroxylase) SB - IM MH - 5' Untranslated Regions/*genetics MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Ethnic Groups/genetics/statistics & numerical data MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Menopause MH - Odds Ratio MH - *Polymorphism, Restriction Fragment Length MH - Risk MH - Steroid 17-alpha-Hydroxylase/*genetics EDAT- 2009/12/17 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/17 06:00 PHST- 2009/12/03 [received] PHST- 2009/12/04 [accepted] PHST- 2009/12/15 [aheadofprint] AID - 10.1007/s10549-009-0679-4 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):221-7. Epub 2009 Dec 15. PMID- 19969469 OWN - NLM STAT- MEDLINE DA - 20100810 DCOM- 20101115 IS - 1879-0461 (Electronic) IS - 1040-8428 (Linking) VI - 75 IP - 3 DP - 2010 Sep TI - Tumour markers predictive of successful treatment of breast cancer with primary endocrine therapy in patients over 70 years old: a prospective study. PG - 249-56 AB - We report a prospective study of women over 70 years of age with early breast cancer who had primary endocrine treatment. Core biopsies of the cancer were taken at diagnosis and assessed using immunohistochemistry for oestrogen receptor (ER), progesterone receptor (PgR), epidermal growth factor receptor (EGFR), pS2, cyclin D1, p21, p53, HER2 and MIB1 (Ki67). Outcome analysis was performed at a median follow-up of 70 months. Correlation was sought between tumour marker measurements and disease control. When all patients were considered, a significant relationship was found between the absence of ER and PgR, the presence of p53 and EGFR, and high MIB1 and treatment failure. However, for the ER positive cancers, no other marker predicted treatment failure or relapse. There remains an important clinical need to identify those ER positive breast cancers that will not respond to endocrine treatment, and those in which the response will be short-lived. CI - Crown Copyright 2009. Published by Elsevier Ireland Ltd. All rights reserved. AD - Breast Surgery, Glenfield Hospital, University Hospitals of Leicester NHS Trust, Groby Road, Leicester, LE3 9QP, UK. anne.stotter@uhl-tr.nhs.uk FAU - Stotter, Anne AU - Stotter A FAU - Walker, Rosemary AU - Walker R LA - eng PT - Journal Article DEP - 20091206 PL - Netherlands TA - Crit Rev Oncol Hematol JT - Critical reviews in oncology/hematology JID - 8916049 RN - 0 (Antineoplastic Agents, Hormonal) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Markers, Biological) RN - 0 (Tumor Suppressor Protein p53) RN - 10540-29-1 (Tamoxifen) RN - EC 2.7.10.1 (Receptor, Epidermal Growth Factor) RN - EC 6.3.2.19 (MIB1 protein, human) RN - EC 6.3.2.19 (Ubiquitin-Protein Ligases) SB - IM MH - Aged MH - Aged, 80 and over MH - Antineoplastic Agents, Hormonal/*therapeutic use MH - Biopsy MH - Breast Neoplasms/*drug therapy/genetics/metabolism/pathology MH - Female MH - Humans MH - Immunohistochemistry MH - Receptor, Epidermal Growth Factor/biosynthesis/genetics MH - Receptors, Estrogen/biosynthesis/genetics MH - Receptors, Progesterone/biosynthesis/genetics MH - Tamoxifen/*therapeutic use MH - Treatment Outcome MH - Tumor Markers, Biological/*analysis MH - Tumor Suppressor Protein p53/biosynthesis/genetics MH - Ubiquitin-Protein Ligases/biosynthesis/genetics EDAT- 2009/12/09 06:00 MHDA- 2010/11/16 06:00 CRDT- 2009/12/09 06:00 PHST- 2009/04/17 [received] PHST- 2009/10/21 [revised] PHST- 2009/10/30 [accepted] PHST- 2009/12/06 [aheadofprint] AID - S1040-8428(09)00222-4 [pii] AID - 10.1016/j.critrevonc.2009.10.008 [doi] PST - ppublish SO - Crit Rev Oncol Hematol. 2010 Sep;75(3):249-56. Epub 2009 Dec 6. PMID- 19949857 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Dietary acrylamide intake and estrogen and progesterone receptor-defined postmenopausal breast cancer risk. PG - 199-210 AB - Acrylamide, a potential human carcinogen, has been discovered in a variety of heat-treated carbohydrate-rich food products. Previously, dietary acrylamide intake was shown to be associated with endocrine-related cancers in humans. We assessed the association between dietary acrylamide intake and risk of postmenopausal breast cancer stratified by estrogen and progesterone receptor status. This study was embedded within the Netherlands Cohort Study on diet and cancer, which was initiated in 1986 enrolling 62,573 women aged 55-69 years at baseline. After 13.3 years of follow-up, 2225 incident breast cancer cases were ascertained, with hormone receptor status information for 43%. Cox proportional hazards analysis was applied to determine hazard ratios in quintiles of dietary acrylamide intake stratifying on estrogen receptor (ER) and progesterone receptor (PR) and smoking status. No association was observed for overall breast cancer or receptor-negative breast cancer risk, irrespective of smoking status. A statistically non-significantly increased risk of ER positive, PR positive and joint receptor-positive breast cancer was found in never-smoking women. The multivariable-adjusted hazard ratios were 1.31 (95% CI: 0.87-1.97, P (trend) = 0.26) for ER+, 1.47 (0.86-2.51, P (trend) = 0.14) for PR+, and 1.43 (0.83-2.46, P (trend) = 0.16) for ER+PR+, when comparing women in the highest quintile of acrylamide intake (median 36.8 microg/day) to women in the lowest (median 9.5 microg/day). This study showed some indications of a positive association between dietary acrylamide intake and receptor-positive breast cancer risk in postmenopausal never-smoking women. Further studies are needed to confirm or refute our observations. AD - Department of Epidemiology, GROW-School for Oncology and Developmental Biology, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. FAU - Pedersen, Grete S AU - Pedersen GS FAU - Hogervorst, Janneke G F AU - Hogervorst JG FAU - Schouten, Leo J AU - Schouten LJ FAU - Konings, Erik J M AU - Konings EJ FAU - Goldbohm, R Alexandra AU - Goldbohm RA FAU - van den Brandt, Piet A AU - van den Brandt PA LA - eng PT - Journal Article PT - Multicenter Study DEP - 20091201 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Acrylamides) RN - 0 (Carcinogens, Environmental) RN - 0 (Estrogens) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 57-83-0 (Progesterone) SB - IM MH - Acrylamides/*adverse effects/analysis MH - Aged MH - Breast Neoplasms/chemically induced/chemistry/*epidemiology MH - Carcinogens, Environmental/*adverse effects/analysis MH - Cohort Studies MH - *Diet MH - *Estrogens MH - Female MH - Food Habits MH - Humans MH - Incidence MH - Middle Aged MH - Neoplasms, Hormone-Dependent/chemically induced/chemistry/*epidemiology MH - Netherlands/epidemiology MH - *Postmenopause MH - *Progesterone MH - Proportional Hazards Models MH - Receptors, Estrogen/*analysis MH - Receptors, Progesterone/*analysis MH - Risk MH - Smoking/epidemiology EDAT- 2009/12/02 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/02 06:00 PHST- 2009/08/24 [received] PHST- 2009/11/10 [accepted] PHST- 2009/12/01 [aheadofprint] AID - 10.1007/s10549-009-0642-4 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):199-210. Epub 2009 Dec 1. PMID- 19949855 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - SULT1A1 R213H polymorphism and breast cancer risk: a meta-analysis based on 8,454 cases and 11,800 controls. PG - 193-8 AB - The SULT1A1 R213H polymorphism is suggested to be implicated in the development and progression of breast cancer. However, the published findings are inconsistent. We therefore performed a meta-analysis of 8,454 breast cancer cases and 11,800 controls from 14 published case-control studies. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association of the R213H polymorphism with breast cancer risk. Overall, our results suggested that there is no significant relationship between SULT1A1 R213H polymorphism and the risk of breast cancer. However, further ethnic population analysis revealed a significantly increased risk of breast cancer for HH allele carriers among Asians (for HH vs. RR: OR = 2.27, 95% CI = 1.11-4.63, P (heterogeneity) = 0.63; for the recessive model: OR = 2.03, 95% CI = 1.00-4.41, P (heterogeneity) = 0.62). Taken together, this meta-analysis suggests that the SULT1A1 R213H may be a low-penetrant risk factor for developing breast cancer in Asian population. AD - Department of Epidemiology and Biostatistics, Nanjing Medical University, 210029 Nanjing, China. FAU - Wang, Zhanwei AU - Wang Z FAU - Fu, Yuanyuan AU - Fu Y FAU - Tang, Chunbo AU - Tang C FAU - Lu, Su AU - Lu S FAU - Chu, Wen-ming AU - Chu WM LA - eng PT - Journal Article PT - Meta-Analysis DEP - 20091201 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Codon) RN - 0 (Neoplasm Proteins) RN - EC 2.8.2.1 (Arylsulfotransferase) RN - EC 2.8.2.1 (SULT1A1 protein, human) SB - IM MH - Alleles MH - Amino Acid Substitution MH - Arylsulfotransferase/*genetics MH - Asia/epidemiology MH - Asian Continental Ancestry Group/genetics MH - Breast Neoplasms/*epidemiology/ethnology/genetics MH - Case-Control Studies MH - Codon/genetics MH - Europe/epidemiology MH - European Continental Ancestry Group/genetics MH - Female MH - Gene Frequency MH - Genetic Predisposition to Disease MH - Genotype MH - Humans MH - Neoplasm Proteins/*genetics MH - Odds Ratio MH - Penetrance MH - *Polymorphism, Single Nucleotide EDAT- 2009/12/02 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/12/02 06:00 PHST- 2009/11/10 [received] PHST- 2009/11/11 [accepted] PHST- 2009/12/01 [aheadofprint] AID - 10.1007/s10549-009-0648-y [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):193-8. Epub 2009 Dec 1. PMID- 19941162 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - High-throughput resequencing in the diagnosis of BRCA1/2 mutations using oligonucleotide resequencing microarrays. PG - 287-97 AB - Breast cancer is the most frequent form of carcinoma in European females (incidence 65 per 100,000). In about 10% of all cases, pedigree analysis predicts a hereditary breast-ovarian cancer syndrome (HBOC) to be causative for the disease. Frequently, mutations in two genes, BRCA1 (Chr. 17q21) and BRCA2 (Chr. 13q12), are associated with HBOC. In females, mutations in these genes result in a lifetime risk of 80-85% for breast cancer and 54% (BRCA1) or 23% (BRCA2) for ovarian cancer. Current genetic diagnostic tools for BRCA1 and BRCA2 remain laborious and expensive. Here, we present the first oligonucleotide resequencing microarray covering the complete coding sequence of both genes. In total, 36 previously characterized DNAs were resequenced; all 11 patients with single-nucleotide mutations and, due to a special mutational design, eight patients with heterozygous deletions were detected correctly. In total, 47 different single-nucleotide variants (SNVs) were found. A newly developed software, SeqC, reduced the number of ambiguous calls with the help of a statistical module comparing the acquired data to an online-database. SeqC improved the average call rate to 99% (GSeq: 97%) and reduced time and efforts for manual analysis. SeqC confirmed the results obtained by GSeq and found an additional 33 sequences changes representing 14 SNVs. In total, 945 kb were screened and the overall turnaround time for each patient took approximately 3 days, including analysis. AD - Department of Medical Genetics, University of Tubingen, Calwer Str 7, 72076 Tubingen, Germany. FAU - Schroeder, Christopher AU - Schroeder C FAU - Stutzmann, Fanny AU - Stutzmann F FAU - Weber, Bernhard H F AU - Weber BH FAU - Riess, Olaf AU - Riess O FAU - Bonin, Michael AU - Bonin M LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091126 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (DNA, Neoplasm) SB - IM MH - Breast Neoplasms/*genetics MH - Carcinoma/*genetics MH - DNA Mutational Analysis/*methods MH - DNA, Neoplasm/*genetics MH - Female MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Genetic Testing/methods MH - Heterozygote MH - *High-Throughput Screening Assays MH - Humans MH - Neoplastic Syndromes, Hereditary/*genetics MH - *Oligonucleotide Array Sequence Analysis MH - Ovarian Neoplasms/genetics MH - Polymorphism, Single Nucleotide MH - Sequence Analysis, DNA/*methods MH - Software MH - Time Factors EDAT- 2009/11/27 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/11/27 06:00 PHST- 2009/09/27 [received] PHST- 2009/11/05 [accepted] PHST- 2009/11/26 [aheadofprint] AID - 10.1007/s10549-009-0639-z [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):287-97. Epub 2009 Nov 26. PMID- 19939368 OWN - NLM STAT- MEDLINE DA - 20100927 DCOM- 20101103 IS - 1556-5653 (Electronic) IS - 0015-0282 (Linking) VI - 94 IP - 5 DP - 2010 Oct TI - Cancer risk among infertile women with androgen excess or menstrual disorders (including polycystic ovary syndrome). PG - 1787-92 AB - OBJECTIVE: To define relationships of androgen excesses to cancer risk. DESIGN: Retrospective cohort study. SETTING: Five large infertility practices. PATIENT(S): Among 12,193 women evaluated for infertility during 1965-1988 and traced for cancer incidence through 1999, 2,560 had androgen excess or menstrual disorders; among these, 412 met established criteria for polycystic ovary syndrome. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Cancer incidence. Derivation of standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for cancer risk comparisons with the general population and rate ratios (RRs) for comparisons with other infertility patients. RESULT(S): Androgen excess/menstrual disorder patients showed significant SIRs for breast (1.31; 95% CI, 1.05-1.62) and uterine (2.02; 95% CI, 1.13-3.34) cancers and melanoma (1.96; 95% CI, 1.12-3.18). Significant associations for breast and uterine cancers were restricted to primary infertility patients (respective SIRs of 1.53 and 3.48). After adjustment for other cancer predictors, the only excess risk was for uterine cancer among primary infertility patients. Compared with women with secondary infertility and no androgen excess/menstrual disorder, those with primary infertility and a disorder had an RR of 1.88 (95% CI, 0.82-4.32). Cancer risks among the women with polycystic ovary syndrome or androgen excess disorders appeared to be similar to those in the more comprehensive group. CONCLUSION(S): Previous findings linking androgen excess disorders to elevated uterine cancer risks might largely reflect underlying risk profiles. CI - Published by Elsevier Inc. AD - National Cancer Institute, Rockville, Maryland, USA. brinton@nih.gov FAU - Brinton, Louise A AU - Brinton LA FAU - Moghissi, Kamran S AU - Moghissi KS FAU - Westhoff, Carolyn L AU - Westhoff CL FAU - Lamb, Emmet J AU - Lamb EJ FAU - Scoccia, Bert AU - Scoccia B LA - eng PT - Journal Article PT - Research Support, N.I.H., Intramural DEP - 20091125 PL - United States TA - Fertil Steril JT - Fertility and sterility JID - 0372772 SB - IM MH - Adult MH - Breast Neoplasms/epidemiology MH - Cohort Studies MH - Female MH - Follow-Up Studies MH - Humans MH - Hyperandrogenism/*complications MH - Incidence MH - Infertility, Female/*complications MH - Melanoma/epidemiology MH - Menstruation Disturbances/*complications MH - Polycystic Ovary Syndrome/*complications MH - Retrospective Studies MH - Risk Factors MH - Skin Neoplasms/epidemiology MH - Uterine Neoplasms/*epidemiology PMC - PMC2888728 MID - NIHMS152392 OID - NLM: NIHMS152392 [Available on 10/01/11] OID - NLM: PMC2888728 [Available on 10/01/11] EDAT- 2009/11/27 06:00 MHDA- 2010/11/04 06:00 CRDT- 2009/11/27 06:00 PMCR- 2011/10/01 PHST- 2009/04/24 [received] PHST- 2009/09/30 [revised] PHST- 2009/10/07 [accepted] PHST- 2009/11/25 [aheadofprint] AID - S0015-0282(09)03872-2 [pii] AID - 10.1016/j.fertnstert.2009.10.012 [doi] PST - ppublish SO - Fertil Steril. 2010 Oct;94(5):1787-92. Epub 2009 Nov 25. PMID- 19921428 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Pooled analysis indicates that the GSTT1 deletion, GSTM1 deletion, and GSTP1 Ile105Val polymorphisms do not modify breast cancer risk in BRCA1 and BRCA2 mutation carriers. PG - 281-5 AB - The GSTP1, GSTM1, and GSTT1 detoxification genes all have functional polymorphisms that are common in the general population. A single study of 320 BRCA1/2 carriers previously assessed their effect in BRCA1 or BRCA2 mutation carriers. This study showed no evidence for altered risk of breast cancer for individuals with the GSTT1 and GSTM1 deletion variants, but did report that the GSTP1 Ile105Val (rs1695) variant was associated with increased breast cancer risk in carriers. We investigated the association between these three GST polymorphisms and breast cancer risk using existing data from 718 women BRCA1 and BRCA2 mutation carriers from Australia, the UK, Canada, and the USA. Data were analyzed within a proportional hazards framework using Cox regression. There was no evidence to show that any of the polymorphisms modified disease risk for BRCA1 or BRCA2 carriers, and there was no evidence for heterogeneity between sites. These results support the need for replication studies to confirm or refute hypothesis-generating studies. AD - Division of Genetics and Population Health, Queensland Institute of Medical Research, 300 Herston Rd, Herston 4006, Australia. FAU - Spurdle, Amanda B AU - Spurdle AB FAU - Fahey, Paul AU - Fahey P FAU - Chen, Xiaoqing AU - Chen X FAU - McGuffog, Lesley AU - McGuffog L CN - kConFab FAU - Easton, Douglas AU - Easton D FAU - Peock, Susan AU - Peock S FAU - Cook, Margaret AU - Cook M CN - EMBRACE FAU - Simard, Jacques AU - Simard J CN - INHERIT FAU - Rebbeck, Tim R AU - Rebbeck TR CN - MAGIC FAU - Antoniou, Antonis C AU - Antoniou AC FAU - Chenevix-Trench, Georgia AU - Chenevix-Trench G LA - eng GR - C1287/A10118/Cancer Research UK/United Kingdom GR - C1287/A8874/Cancer Research UK/United Kingdom GR - R01-CA083855/CA/NCI NIH HHS/United States GR - R01-CA102776/CA/NCI NIH HHS/United States GR - Canadian Institutes of Health Research/Canada PT - Journal Article PT - Meta-Analysis PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20091118 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - EC 2.5.1.- (glutathione S-transferase T1) RN - EC 2.5.1.18 (GSTP1 protein, human) RN - EC 2.5.1.18 (Glutathione S-Transferase pi) RN - EC 2.5.1.18 (Glutathione Transferase) RN - EC 2.5.1.18 (glutathione S-transferase M1) SB - IM MH - Amino Acid Substitution MH - Breast Neoplasms/*epidemiology/genetics MH - Ethnic Groups/genetics/statistics & numerical data MH - Female MH - *Gene Deletion MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Genetic Predisposition to Disease MH - Genotype MH - Glutathione S-Transferase pi/*genetics MH - Glutathione Transferase/*genetics MH - Heterozygote MH - Humans MH - Incidence MH - Neoplastic Syndromes, Hereditary/*genetics MH - *Polymorphism, Single Nucleotide MH - Proportional Hazards Models MH - Risk IR - Peock S FIR - Peock, Susan IR - Cook M FIR - Cook, Margaret IR - Oliver C FIR - Oliver, Clare IR - Frost D FIR - Frost, Debra IR - Gregory H FIR - Gregory, Helen IR - Miedzybrodzka Z FIR - Miedzybrodzka, Zosia IR - Morrison P FIR - Morrison, Patrick IR - Cole T FIR - Cole, Trevor IR - McKeown C FIR - McKeown, Carole IR - Taylor A FIR - Taylor, Amy IR - Donaldson A FIR - Donaldson, Alan IR - Paterson J FIR - Paterson, Joan IR - Murray A FIR - Murray, Alexandra IR - Rogers M FIR - Rogers, Mark IR - McCann E FIR - McCann, Emma IR - Kennedy J FIR - Kennedy, John IR - Barton D FIR - Barton, David IR - Porteous M FIR - Porteous, Mary IR - Brewer C FIR - Brewer, Carole IR - Kivuva E FIR - Kivuva, Emma IR - Searle A FIR - Searle, Anne IR - Goodman S FIR - Goodman, Selina IR - Davidson R FIR - Davidson, Rosemarie IR - Murday V FIR - Murday, Victoria IR - Bradshaw N FIR - Bradshaw, Nicola IR - Snadden L FIR - Snadden, Lesley IR - Longmuir M FIR - Longmuir, Mark IR - Watt C FIR - Watt, Catherine IR - Izatt L FIR - Izatt, Louise IR - Pichert G FIR - Pichert, Gabriella IR - Langman C FIR - Langman, Caroline IR - Dorkins H FIR - Dorkins, Huw IR - Barwell J FIR - Barwell, Julian IR - Chu C FIR - Chu, Carol IR - Bishop T FIR - Bishop, Tim IR - Miller J FIR - Miller, Julie IR - Ellis I FIR - Ellis, Ian IR - Evans DG FIR - Evans, D Gareth IR - Lalloo F FIR - Lalloo, Fiona IR - Holt F FIR - Holt, Felicity IR - Male A FIR - Male, Alison IR - Robinson A FIR - Robinson, Anne IR - Gardiner C FIR - Gardiner, Carol IR - Douglas F FIR - Douglas, Fiona IR - Walker L FIR - Walker, Lisa IR - McLeod D FIR - McLeod, Diane IR - Eeles R FIR - Eeles, Ros IR - Shanley S FIR - Shanley, Susan IR - Rahman N FIR - Rahman, Nazneen IR - Houlston R FIR - Houlston, Richard IR - Bancroft E FIR - Bancroft, Elizabeth IR - D'Mello L FIR - D'Mello, Lucia IR - Page E FIR - Page, Elizabeth IR - Ardern-Jones A FIR - Ardern-Jones, Audrey IR - Mitra A FIR - Mitra, Anita IR - Cook J FIR - Cook, Jackie IR - Quarrell O FIR - Quarrell, Oliver IR - Bardsley C FIR - Bardsley, Cathryn IR - Hodgson S FIR - Hodgson, Shirley IR - Goff S FIR - Goff, Sheila IR - Brice G FIR - Brice, Glen IR - Winchester L FIR - Winchester, Lizzie IR - Eccles D FIR - Eccles, Diana IR - Lucassen A FIR - Lucassen, Anneke IR - Crawford G FIR - Crawford, Gillian IR - Tyler E FIR - Tyler, Emma IR - McBride D FIR - McBride, Donna IR - Simard J FIR - Simard, Jacques IR - Durocher F FIR - Durocher, Francine IR - Laframboise R FIR - Laframboise, Rachel IR - Plante M FIR - Plante, Marie IR - Bridge P FIR - Bridge, Peter IR - Parboosingh J FIR - Parboosingh, Jilian IR - Chiquette J FIR - Chiquette, Jocelyne IR - Lesperance B FIR - Lesperance, Bernard IR - Simard J FIR - Simard, Jacques IR - Joanne L FIR - Joanne, L IR - Becky A FIR - Becky, Althaus IR - Ethington G FIR - Ethington, Gaby IR - Noll C FIR - Noll, Claire IR - Plon S FIR - Plon, Sharon IR - Tung N FIR - Tung, Nadine IR - Sand S FIR - Sand, Sharon IR - Weitzel JN FIR - Weitzel, Jeffrey N IR - Snyder C FIR - Snyder, Carrie IR - Lynch HT FIR - Lynch, Henry T IR - Watson P FIR - Watson, Patrice IR - Stoeckert K FIR - Stoeckert, Kathryn IR - Garber JE FIR - Garber, Judy E IR - Crankshaw S FIR - Crankshaw, Sydnee IR - Schildkraut J FIR - Schildkraut, Joellen IR - O'Neill SM FIR - O'Neill, Suzanne M IR - Selkirk C FIR - Selkirk, Christina IR - Rubinstein WS FIR - Rubinstein, Wendy S IR - Daly MB FIR - Daly, Mary B IR - Godwin A FIR - Godwin, Andrew IR - Chenevix-Trench G FIR - Chenevix-Trench, Georgia IR - Isaacs C FIR - Isaacs, Claudine IR - Seldon J FIR - Seldon, Joyce IR - Ganz PA FIR - Ganz, Patricia A IR - Wadum L FIR - Wadum, Linda IR - Couch F FIR - Couch, Fergus IR - Cummings S FIR - Cummings, Shelly IR - Olopade O FIR - Olopade, Olufunmilayo IR - Neuhausen SL FIR - Neuhausen, Susan L IR - Steele L FIR - Steele, Linda IR - Domchek S FIR - Domchek, Susan IR - Nathanson K FIR - Nathanson, Katherine IR - Friebel T FIR - Friebel, Tara IR - Rebbeck T FIR - Rebbeck, Timothy IR - Tomlinson G FIR - Tomlinson, Gail IR - Singer C FIR - Singer, Christian IR - Narod SA FIR - Narod, Steven A EDAT- 2009/11/19 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/11/19 06:00 PHST- 2009/10/11 [received] PHST- 2009/10/12 [accepted] PHST- 2009/11/18 [aheadofprint] AID - 10.1007/s10549-009-0601-0 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):281-5. Epub 2009 Nov 18. PMID- 19921424 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Five common single nucleotide polymorphisms in the PALB2 gene and susceptibility to breast cancer in eastern Chinese population. PG - 133-8 AB - Certain rare germline mutations in the PALB2 gene have been confirmed to increase susceptibility to breast cancer in diverse populations, but it has not been very clear that whether some common polymorphic variants in PALB2 also increase breast cancer risk. We conducted a case-control study to validate the association of common variations in the PALB2 gene and breast cancer in eastern Chinese population. A total of six common single nucleotide polymorphisms (rs8053188, rs16940342, rs249954, rs447529, rs249935, and rs3096145), which tagged the known common variants (minor allele frequency >0.1) of PALB2, were genotyped among 660 cases and 756 cancer-free controls by SNPstream assay. Except rs3096145, other five SNPs passed the quality assessment criteria with genotyping call rate >95%. Genotype and allele frequencies were statistically different between cases and controls for PALB2 rs447529 and rs249935. PALB2 rs249935 G allele was related to a 1.21-fold (95% confidence interval = 1.02-1.43) increase in risk for each 'A' allele carried (P = 0.029). Based on the dominant inheritance model tests, we found that compared with rs447529 CC homozygotes, the variant homozygote GG and heterozygote GC carriers had a 0.43-fold decreased risk of breast cancer (95% confidence interval = 0.24-0.78, P = 0.005). Combined with the results of the former study, our findings further verified that some common PALB2 polymorphisms may contribute to the etiology of breast cancer in Chinese women, so other large studies are warranted to confirm these observations in different ethnic populations. AD - Department of Oncology, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Shanghai Medical College, Fudan University, 270 Dong'an Road, Shanghai 200032, People's Republic of China. FAU - Cao, A-Yong AU - Cao AY FAU - Yu, Ke-Da AU - Yu KD FAU - Yin, Wen-Jin AU - Yin WJ FAU - Jin, Wei AU - Jin W FAU - Di, Gen-Hong AU - Di GH FAU - Shen, Zhen-Zhou AU - Shen ZZ FAU - Shao, Zhi-Ming AU - Shao ZM LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091118 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Nuclear Proteins) RN - 0 (PALB2 protein, human) RN - 0 (Tumor Suppressor Proteins) SB - IM MH - Adult MH - Asian Continental Ancestry Group/genetics MH - Breast Neoplasms/*genetics MH - Case-Control Studies MH - Female MH - Gene Frequency MH - Genetic Predisposition to Disease/*genetics MH - Genotype MH - Humans MH - Middle Aged MH - Nuclear Proteins/*genetics MH - *Polymorphism, Single Nucleotide MH - Tumor Suppressor Proteins/*genetics EDAT- 2009/11/19 06:00 MHDA- 2010/11/10 06:00 CRDT- 2009/11/19 06:00 PHST- 2009/05/06 [received] PHST- 2009/11/05 [accepted] PHST- 2009/11/18 [aheadofprint] AID - 10.1007/s10549-009-0637-1 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):133-8. Epub 2009 Nov 18. PMID- 19920276 OWN - NLM STAT- MEDLINE DA - 20091120 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 151 IP - 10 DP - 2009 Nov 17 TI - Evidence-based breast cancer prevention: the importance of individual risk. PG - 750-2 FAU - Kerlikowske, Karla AU - Kerlikowske K LA - eng GR - P50 CA58207/CA/NCI NIH HHS/United States GR - U01CA63740/CA/NCI NIH HHS/United States PT - Editorial PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 SB - AIM SB - IM EIN - Ann Intern Med. 2010 Jan 19;152(2):136 MH - Adult MH - Aged MH - Breast Neoplasms/*prevention & control MH - *Evidence-Based Medicine MH - Female MH - Humans MH - *Mammography MH - Mass Screening/*methods MH - Middle Aged MH - Risk Assessment EDAT- 2009/11/19 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/11/19 06:00 AID - 151/10/750 [pii] AID - 10.1059/0003-4819-151-10-200911170-00012 [doi] PST - ppublish SO - Ann Intern Med. 2009 Nov 17;151(10):750-2. PMID- 19920273 OWN - NLM STAT- MEDLINE DA - 20091120 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 151 IP - 10 DP - 2009 Nov 17 TI - Screening for breast cancer: an update for the U.S. Preventive Services Task Force. PG - 727-37, W237-42 AB - BACKGROUND: This systematic review is an update of evidence since the 2002 U.S. Preventive Services Task Force recommendation on breast cancer screening. PURPOSE: To determine the effectiveness of mammography screening in decreasing breast cancer mortality among average-risk women aged 40 to 49 years and 70 years or older, the effectiveness of clinical breast examination and breast self-examination, and the harms of screening. DATA SOURCES: Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews (through the fourth quarter of 2008), MEDLINE (January 2001 to December 2008), reference lists, and Web of Science searches for published studies and Breast Cancer Surveillance Consortium for screening mammography data. STUDY SELECTION: Randomized, controlled trials with breast cancer mortality outcomes for screening effectiveness, and studies of various designs and multiple data sources for harms. DATA EXTRACTION: Relevant data were abstracted, and study quality was rated by using established criteria. DATA SYNTHESIS: Mammography screening reduces breast cancer mortality by 15% for women aged 39 to 49 years (relative risk, 0.85 [95% credible interval, 0.75 to 0.96]; 8 trials). Data are lacking for women aged 70 years or older. Radiation exposure from mammography is low. Patient adverse experiences are common and transient and do not affect screening practices. Estimates of overdiagnosis vary from 1% to 10%. Younger women have more false-positive mammography results and additional imaging but fewer biopsies than older women. Trials of clinical breast examination are ongoing; trials for breast self-examination showed no reductions in mortality but increases in benign biopsy results. Limitation: Studies of older women, digital mammography, and magnetic resonance imaging are lacking. CONCLUSION: Mammography screening reduces breast cancer mortality for women aged 39 to 69 years; data are insufficient for older women. False-positive mammography results and additional imaging are common. No benefit has been shown for clinical breast examination or breast self-examination. AD - Oregon Health & Science University, Veterans Affairs Medical Center, Portland, OR 97239-3098, USA. nelsonh@ohsu.edu FAU - Nelson, Heidi D AU - Nelson HD FAU - Tyne, Kari AU - Tyne K FAU - Naik, Arpana AU - Naik A FAU - Bougatsos, Christina AU - Bougatsos C FAU - Chan, Benjamin K AU - Chan BK FAU - Humphrey, Linda AU - Humphrey L CN - U.S. Preventive Services Task Force LA - eng GR - 290-02-0024/PHS HHS/United States GR - U01 CA063731-10/CA/NCI NIH HHS/United States GR - U01 CA063736-109001/CA/NCI NIH HHS/United States GR - U01 CA063740-14/CA/NCI NIH HHS/United States GR - U01 CA069976-06/CA/NCI NIH HHS/United States GR - U01 CA070013-05/CA/NCI NIH HHS/United States GR - U01 CA070040-14/CA/NCI NIH HHS/United States GR - U01 CA086076-10S1/CA/NCI NIH HHS/United States GR - U01 CA086082-10/CA/NCI NIH HHS/United States GR - U01CA63731/CA/NCI NIH HHS/United States GR - U01CA63736/CA/NCI NIH HHS/United States GR - U01CA63740/CA/NCI NIH HHS/United States GR - U01CA69976/CA/NCI NIH HHS/United States GR - U01CA70013/CA/NCI NIH HHS/United States GR - U01CA70040/CA/NCI NIH HHS/United States GR - U01CA86076/CA/NCI NIH HHS/United States GR - U01CA86082/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, U.S. Gov't, P.H.S. PT - Review PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 SB - AIM SB - IM CIN - Ann Intern Med. 2010 Nov 2;153(9):618-9; author reply 619. PMID: 21041585 CIN - Ann Intern Med. 2010 Apr 20;152(8):537; author reply 538-9. PMID: 20157109 CIN - Ann Intern Med. 2010 Apr 20;152(8):537-8; author reply 538-9. PMID: 20157111 CIN - Evid Based Med. 2010 Apr;15(2):62-3. PMID: 20436133 CIN - Ann Intern Med. 2010 Apr 20;152(8):538; author reply 538-9. PMID: 20157097 CIN - Ann Intern Med. 2010 Feb 16;152(4):JC-27. PMID: 20157131 MH - Adult MH - Age Factors MH - Aged MH - Anxiety/etiology MH - Breast Neoplasms/*diagnosis/mortality MH - Breast Self-Examination MH - Early Detection of Cancer MH - Female MH - Health Care Costs MH - Humans MH - Magnetic Resonance Imaging/economics MH - Mammography/adverse effects/economics/methods MH - Mass Screening/economics/*methods MH - Middle Aged MH - Palpation/economics MH - Risk Factors RF - 67 PMC - PMC2972726 MID - NIHMS225194 OID - NLM: NIHMS225194 OID - NLM: PMC2972726 EDAT- 2009/11/19 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/11/19 06:00 AID - 151/10/727 [pii] AID - 10.1059/0003-4819-151-10-200911170-00009 [doi] PST - ppublish SO - Ann Intern Med. 2009 Nov 17;151(10):727-37, W237-42. PMID- 19920272 OWN - NLM STAT- MEDLINE DA - 20091120 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 151 IP - 10 DP - 2009 Nov 17 TI - Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. PG - 716-26, W-236 AB - DESCRIPTION: Update of the 2002 U.S. Preventive Services Task Force (USPSTF) recommendation statement on screening for breast cancer in the general population. METHODS: The USPSTF examined the evidence on the efficacy of 5 screening modalities in reducing mortality from breast cancer: film mammography, clinical breast examination, breast self-examination, digital mammography, and magnetic resonance imaging in order to update the 2002 recommendation. To accomplish this update, the USPSTF commissioned 2 studies: 1) a targeted systematic evidence review of 6 selected questions relating to benefits and harms of screening, and 2) a decision analysis that used population modeling techniques to compare the expected health outcomes and resource requirements of starting and ending mammography screening at different ages and using annual versus biennial screening intervals. RECOMMENDATIONS: The USPSTF recommends against routine screening mammography in women aged 40 to 49 years. The decision to start regular, biennial screening mammography before the age of 50 years should be an individual one and take into account patient context, including the patient's values regarding specific benefits and harms. (Grade C recommendation) The USPSTF recommends biennial screening mammography for women between the ages of 50 and 74 years. (Grade B recommendation) The USPSTF concludes that the current evidence is insufficient to assess the additional benefits and harms of screening mammography in women 75 years or older. (I statement) The USPSTF concludes that the current evidence is insufficient to assess the additional benefits and harms of clinical breast examination beyond screening mammography in women 40 years or older. (I statement) The USPSTF recommends against clinicians teaching women how to perform breast self-examination. (Grade D recommendation) The USPSTF concludes that the current evidence is insufficient to assess additional benefits and harms of either digital mammography or magnetic resonance imaging instead of film mammography as screening modalities for breast cancer. (I statement). AD - the U.S. Preventive Services Task Force, Agency for Healthcare Research and Quality, Rockville, Maryland. CN - US Preventive Services Task Force LA - eng PT - Journal Article PT - Practice Guideline PT - Research Support, U.S. Gov't, Non-P.H.S. PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 SB - AIM SB - IM CIN - Ann Intern Med. 2010 Apr 20;152(8):539; author reply 543-4. PMID: 20157108 CIN - Ann Intern Med. 2010 Apr 20;152(8):541-2; author reply 543-4. PMID: 20157105 CIN - Ann Intern Med. 2010 Apr 20;152(8):541; author reply 543-4. PMID: 20157098 CIN - Natl Med J India. 2010 May-Jun;23(3):152-3. PMID: 20949718 CIN - Ann Intern Med. 2010 Apr 20;152(8):539-40; author reply 543-4. PMID: 20157104 CIN - Ann Intern Med. 2010 Apr 20;152(8):540; author reply 543-4. PMID: 20157102 CIN - Ann Intern Med. 2010 Apr 20;152(8):542; author reply 543-4. PMID: 20157100 CIN - Ann Intern Med. 2010 Apr 20;152(8):537-8; author reply 538-9. PMID: 20157111 CIN - Ann Intern Med. 2010 Apr 20;152(8):540-1; author reply 543-4. PMID: 20157101 CIN - Am J Kidney Dis. 2010 Nov;56(5):820-2. PMID: 20605300 CIN - Ann Intern Med. 2010 Apr 20;152(8):542-3; author reply 543-4. PMID: 20157107 EIN - Ann Intern Med. 2010 May 18;152(10):688 EIN - Ann Intern Med. 2010 Feb 2;152(3):199-200 SPIN- Ann Intern Med. 2009 Nov 17;151(10):I44. PMID: 19920254 MH - Adult MH - Age Factors MH - Aged MH - Anxiety/etiology MH - Breast Neoplasms/*diagnosis/mortality MH - Breast Self-Examination MH - Early Detection of Cancer MH - False Positive Reactions MH - Female MH - Health Care Costs MH - Humans MH - Magnetic Resonance Imaging/economics MH - Mammography/adverse effects/economics/methods MH - Mass Screening/economics/*methods MH - Middle Aged MH - Palpation/economics MH - Risk Factors IR - Calonge N FIR - Calonge, Ned IR - Petitti DB FIR - Petitti, Diana B IR - DeWitt TG FIR - DeWitt, Thomas G IR - Dietrich AJ FIR - Dietrich, Allen J IR - Gregory KD FIR - Gregory, Kimberly D IR - Grossman D FIR - Grossman, David IR - Isham G FIR - Isham, George IR - LeFevre ML FIR - LeFevre, Michael L IR - Leipzig RM FIR - Leipzig, Rosanne M IR - Marion LN FIR - Marion, Lucy N IR - Melnyk B FIR - Melnyk, Bernadette IR - Moyer VA FIR - Moyer, Virginia A IR - Ockene JK FIR - Ockene, Judith K IR - Sawaya GF FIR - Sawaya, George F IR - Schwartz JS FIR - Schwartz, J Sanford IR - Wilt T FIR - Wilt, Timothy EDAT- 2009/11/19 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/11/19 06:00 AID - 151/10/716 [pii] AID - 10.1059/0003-4819-151-10-200911170-00008 [doi] PST - ppublish SO - Ann Intern Med. 2009 Nov 17;151(10):716-26, W-236. PMID- 19920271 OWN - NLM STAT- MEDLINE DA - 20091120 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 151 IP - 10 DP - 2009 Nov 17 TI - Systematic review: comparative effectiveness of medications to reduce risk for primary breast cancer. PG - 703-15, W-226-35 AB - BACKGROUND: Trials demonstrate the efficacy of medications to reduce the risk for invasive breast cancer. PURPOSE: To summarize benefits and harms of tamoxifen citrate, raloxifene, and tibolone to reduce the risk for primary breast cancer. DATA SOURCES: MEDLINE and Cochrane databases from inception to January 2009, Web of Science, trial registries, and manufacturer information. STUDY SELECTION: Predefined eligibility criteria were used to select articles. English-language reports of randomized, controlled trials (RCTs) for benefits and RCTs and observational studies for harms were included. DATA EXTRACTION: Two reviewers assessed study data, quality, and applicability. DATA SYNTHESIS: Seven placebo-controlled RCTs and 1 head-to-head trial provide results for main outcomes. Tamoxifen (risk ratio, 0.70 [95% CI, 0.59 to 0.82]; 4 trials), raloxifene (risk ratio, 0.44 [CI, 0.27 to 0.71]; 2 trials), and tibolone (risk ratio, 0.32 [CI, 0.13 to 0.80]; 1 trial) reduce risk for invasive breast cancer compared with placebo by 7 to 10 per 1000 women per year. Tamoxifen and raloxifene reduce estrogen receptor-positive breast cancer but not estrogen receptor-negative breast cancer, noninvasive breast cancer, or mortality. All medications reduce fractures. Tamoxifen (risk ratio, 1.93 [CI, 1.41 to 2.64]; 4 trials) and raloxifene (risk ratio, 1.60 [CI, 1.15 to 2.23]; 2 trials) increase thromboembolic events by 4 to 7 per 1000 women per year; raloxifene causes fewer events than tamoxifen. Tamoxifen increases risk for endometrial cancer (risk ratio, 2.13 [CI, 1.36 to 3.32]; 3 trials) compared with placebo by 4 per 1000 women per year and causes cataracts compared with raloxifene. Tibolone causes strokes in older women. LIMITATIONS: Bias, trial heterogeneity, and a dearth of head-to-head trials limit this review. Data are lacking on doses, duration, and timing of the medications; long-term effects; and nonwhite and premenopausal women. CONCLUSION: Three medications reduce risk for primary breast cancer but increase risk for thromboembolic events (tamoxifen, raloxifene), endometrial cancer (tamoxifen), or stroke (tibolone). AD - Oregon Health & Science University, Veterans Affairs Medical Center, Portland, OR 97239-3098, USA. nelsonh@ohsu.edu FAU - Nelson, Heidi D AU - Nelson HD FAU - Fu, Rongwei AU - Fu R FAU - Griffin, Jessica C AU - Griffin JC FAU - Nygren, Peggy AU - Nygren P FAU - Smith, M E Beth AU - Smith ME FAU - Humphrey, Linda AU - Humphrey L LA - eng GR - 290-2007-10057-1/PHS HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PT - Review PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 RN - 0 (Estrogen Receptor Modulators) RN - 0 (Norpregnenes) RN - 10540-29-1 (Tamoxifen) RN - 5630-53-5 (tibolone) RN - 84449-90-1 (Raloxifene) SB - AIM SB - IM CIN - Ann Intern Med. 2010 Mar 16;152(6):JC3-4. PMID: 20231558 CIN - Evid Based Med. 2010 Aug;15(4):122. PMID: 20682726 MH - Breast Neoplasms/*prevention & control MH - Endometrial Neoplasms/chemically induced MH - Estrogen Receptor Modulators/adverse effects/*therapeutic use MH - Female MH - Fractures, Bone/prevention & control MH - Humans MH - Norpregnenes/adverse effects/*therapeutic use MH - Raloxifene/adverse effects/*therapeutic use MH - Stroke/chemically induced MH - Tamoxifen/adverse effects/*therapeutic use MH - Thromboembolism/chemically induced RF - 73 EDAT- 2009/11/19 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/11/19 06:00 AID - 151/10/703 [pii] AID - 10.1059/0003-4819-151-10-200911170-00147 [doi] PST - ppublish SO - Ann Intern Med. 2009 Nov 17;151(10):703-15, W-226-35. PMID- 19920254 OWN - NLM STAT- MEDLINE DA - 20091120 DCOM- 20101116 IS - 1539-3704 (Electronic) IS - 0003-4819 (Linking) VI - 151 IP - 10 DP - 2009 Nov 17 TI - Summaries for patients. Screening for breast cancer: U.S. Preventive Services Task Force recommendations. PG - I44 LA - eng PT - Journal Article PL - United States TA - Ann Intern Med JT - Annals of internal medicine JID - 0372351 SB - AIM SB - IM ORI - Ann Intern Med. 2009 Nov 17;151(10):716-26, W-236. PMID: 19920272 MH - Adult MH - Age Factors MH - Aged MH - Breast Neoplasms/*diagnosis/mortality MH - Breast Self-Examination MH - Early Detection of Cancer MH - Female MH - Health Care Costs MH - Humans MH - Magnetic Resonance Imaging/economics MH - Mammography/economics/methods MH - Mass Screening/economics/*methods MH - Middle Aged MH - Palpation/economics MH - Risk Factors EDAT- 2009/11/19 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/11/19 06:00 AID - 151/10/I-44 [pii] AID - 10.1059/0003-4819-151-10-200911170-00002 [doi] PST - ppublish SO - Ann Intern Med. 2009 Nov 17;151(10):I44. PMID- 19912305 OWN - NLM STAT- MEDLINE DA - 20100607 DCOM- 20101029 IS - 1365-2354 (Electronic) IS - 0961-5423 (Linking) VI - 19 IP - 3 DP - 2010 May TI - Attitude towards genetic testing for breast cancer susceptibility: a comparison of affected and unaffected women. PG - 360-8 AB - The objective of this study is to evaluate women's awareness and interest in genetic testing for breast cancer risk, to identify socio-demographic factors, to analyse the reasons for wanting or not wanting to be tested and finally to determine whether breast cancer patients and healthy women have different attitudes towards genetic testing. Consecutive series of 879 women without and with breast cancer participated in a 20-item self-completing questionnaire. Among breast cancer patients, 57% answered that they would definitely or probably accept being tested, compared with 84% of women without breast cancer. At the multiple logistic regression analysis only to have a diagnosis of breast cancer conditioned significantly the interest to have genetic testing. Surprisingly, a family history of breast cancer was found to have no significant impact. The most frequently cited reason for being interested in genetic testing was 'to learn about your children's risk'. Although women's awareness about breast cancer genes is inadequate, the interest in genetic testing is substantial and higher both in healthy women and in women with breast cancer. These results provide important indications for the development of educational strategies. AD - Experimental Oncology Department, Cancer Institute of Bari, Bari, Italy. m.bruno@oncologico.bari.it FAU - Bruno, M AU - Bruno M FAU - Digennaro, M AU - Digennaro M FAU - Tommasi, S AU - Tommasi S FAU - Stea, B AU - Stea B FAU - Danese, T AU - Danese T FAU - Schittulli, F AU - Schittulli F FAU - Paradiso, A AU - Paradiso A LA - eng PT - Journal Article DEP - 20091113 PL - England TA - Eur J Cancer Care (Engl) JT - European journal of cancer care JID - 9301979 SB - N MH - Adult MH - Aged MH - *Attitude to Health MH - Awareness MH - Breast Neoplasms/*diagnosis/*genetics/psychology MH - Family MH - Female MH - Genetic Predisposition to Disease MH - Genetic Testing/*psychology MH - Humans MH - Logistic Models MH - Mass Screening/methods/psychology MH - Middle Aged MH - Questionnaires MH - Socioeconomic Factors MH - Young Adult EDAT- 2009/11/17 06:00 MHDA- 2010/10/30 06:00 CRDT- 2009/11/17 06:00 PHST- 2009/11/13 [aheadofprint] AID - ECC1067 [pii] AID - 10.1111/j.1365-2354.2009.01067.x [doi] PST - ppublish SO - Eur J Cancer Care (Engl). 2010 May;19(3):360-8. Epub 2009 Nov 13. PMID- 19911270 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101109 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 123 IP - 1 DP - 2010 Aug TI - Prognostic impact of ALDH1 in breast cancer: a story of stem cells and tumor microenvironment. PG - 97-108 AB - The concept of cancer cells being hierarchically organized and arising from their own progenitor stem cells will have important implications on cancer therapy. If this hypothesis were to be true then the paucity of estrogen receptors in stem cells as well as their inherent drug resistance mechanisms pose a challenge to current targeted therapies. In this study, we sought to examine the prognostic relevance of ALDH1, a putative cancer stem cell marker, by immunohistochemistry. The four cohorts analyzed included an adjuvantly treated series of 245 invasive cancers, a neoadjuvantly treated series of 34 cases, and two series of 58 and 40 triple negative cases, respectively. Both tumor cell and stromal expression for ALDH1 was evaluated, where possible. Tumor cell ALDH1 expression significantly correlated only with basal-like and HER2 tumor types in the adjuvant series and tumor grade in the neoadjuvant cohort. No significant enrichment for ALDH1 positive cells was observed in the postneoadjuvant therapy specimens compared to pretreatment samples. On the other hand, high degree of stromal expression was significantly associated with best disease-free survival as well as a trend for overall survival. The association of stromal expression was confirmed in an independent cohort of triple negative cases. The novel finding is that tumor microenvironment may play a significant role in determining the prognostic impact of stem/progenitor cells in human breast tumors. AD - Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 46202, USA. FAU - Resetkova, Erika AU - Resetkova E FAU - Reis-Filho, Jorge S AU - Reis-Filho JS FAU - Jain, Rohit K AU - Jain RK FAU - Mehta, Rutika AU - Mehta R FAU - Thorat, Mangesh A AU - Thorat MA FAU - Nakshatri, Harikrishna AU - Nakshatri H FAU - Badve, Sunil AU - Badve S LA - eng PT - Journal Article DEP - 20091113 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Antineoplastic Agents) RN - 0 (Isoenzymes) RN - 0 (Receptors, Estrogen) RN - 0 (Receptors, Progesterone) RN - 0 (Tumor Markers, Biological) RN - EC 1.2.1.- (aldehyde dehydrogenase 1) RN - EC 1.2.1.3 (Aldehyde Dehydrogenase) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM CIN - Breast Cancer Res Treat. 2010 Aug;123(1):109-11. PMID: 19946740 MH - Aldehyde Dehydrogenase/*biosynthesis MH - Antineoplastic Agents/therapeutic use MH - Breast Neoplasms/drug therapy/*metabolism/pathology MH - Chemotherapy, Adjuvant MH - Extracellular Matrix/*metabolism MH - Female MH - Gene Expression MH - Humans MH - Immunohistochemistry MH - Isoenzymes/*biosynthesis MH - Kaplan-Meiers Estimate MH - Neoadjuvant Therapy MH - Neoplasm Staging MH - Neoplastic Stem Cells/*metabolism MH - Prognosis MH - Receptor, erbB-2/metabolism MH - Receptors, Estrogen/metabolism MH - Receptors, Progesterone/metabolism MH - Tissue Array Analysis MH - Tumor Markers, Biological/*analysis EDAT- 2009/11/17 06:00 MHDA- 2010/11/10 06:00 CRDT- 2009/11/14 06:00 PHST- 2009/08/13 [received] PHST- 2009/10/07 [accepted] PHST- 2009/11/13 [aheadofprint] AID - 10.1007/s10549-009-0619-3 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;123(1):97-108. Epub 2009 Nov 13. PMID- 19894111 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - Identification and comprehensive characterization of large genomic rearrangements in the BRCA1 and BRCA2 genes. PG - 733-43 AB - Large genomic rearrangements are estimated to account for approximately 5-10% of all disease-causing mutations in BRCA1 and BRCA2 genes in patients with hereditary breast and ovarian cancer syndrome (HBOC). We use MRC-Holland Multiplex Ligation-dependent Probe Amplification (MLPA) to screen for such rearrangements in patients with HBOC and as a first step in our genetic testing workflow. The technique was applied to a set of 310 independent patients and detected eight different copy number alterations, corresponding to 2.6% of the studied samples. MLPA was also found to identify point mutations located in probe sequences. As commercial MLPA tests are not suitable for determining the specific breakpoints or for defining the exact extent of rearrangements, we applied a set of different complementary techniques to characterize these genetic alterations with greater precision. Long-range PCR amplification, RNA analysis, SNP-array chips, non-commercial MLPA probes, and FISH analysis were used to fully define the extent and mechanism of each alteration. In BRCA1, six rearrangements were characterized: deletion of E22, duplication of E9-E24, deletion of E16-E23, deletion of E1-E13, deletion of E1-E2 and duplication of E1-E2. In BRCA2, we studied a deletion of E15-E16 and a deletion of E1-E24. To the best of our knowledge, this is the most comprehensive study of the nature and underlying molecular causes of these mutational events in the BRCA1/2 genes. AD - Programa de Diagnostic Molecular de Cancer Hereditari, Laboratori de Recerca Translacional, Institut Catala d'Oncologia-IDIBELL, Hospital Duran i Reynals, Hospitalet de Llobregat, Gran Via s/n, km 2.7, L'Hospitalet de Llobregat, 08907 Barcelona, Spain. FAU - del Valle, Jesus AU - del Valle J FAU - Feliubadalo, Lidia AU - Feliubadalo L FAU - Nadal, Marga AU - Nadal M FAU - Teule, Alex AU - Teule A FAU - Miro, Rosa AU - Miro R FAU - Cuesta, Raquel AU - Cuesta R FAU - Tornero, Eva AU - Tornero E FAU - Menendez, Mireia AU - Menendez M FAU - Darder, Esther AU - Darder E FAU - Brunet, Joan AU - Brunet J FAU - Capella, Gabriel AU - Capella G FAU - Blanco, Ignacio AU - Blanco I FAU - Lazaro, Conxi AU - Lazaro C LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091106 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 SB - IM MH - Adult MH - Base Sequence MH - Breast Neoplasms/*genetics MH - Female MH - *Gene Rearrangement MH - *Genes, BRCA1 MH - *Genes, BRCA2 MH - Genetic Predisposition to Disease MH - *Genome, Human MH - Humans MH - Male MH - Middle Aged MH - Molecular Sequence Data MH - Ovarian Neoplasms/*genetics MH - Pedigree MH - Point Mutation MH - Polymerase Chain Reaction MH - Polymorphism, Single Nucleotide MH - Sequence Homology, Nucleic Acid EDAT- 2009/11/07 06:00 MHDA- 2010/10/27 06:00 CRDT- 2009/11/07 06:00 PHST- 2009/08/26 [received] PHST- 2009/10/20 [accepted] PHST- 2009/11/06 [aheadofprint] AID - 10.1007/s10549-009-0613-9 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):733-43. Epub 2009 Nov 6. PMID- 19863427 OWN - NLM STAT- MEDLINE DA - 20091029 DCOM- 20101116 IS - 1651-2073 (Electronic) IS - 0284-4311 (Linking) VI - 43 IP - 5 DP - 2009 TI - Germline mutation screening of the Saethre-Chotzen-associated genes TWIST1 and FGFR3 in families with BRCA1/2-negative breast cancer. PG - 251-5 AB - Saethre-Chotzen syndrome is one of the most common craniosynostosis syndromes. It is an autosomal dominantly inherited disorder with variable expression that is caused by germline mutations in the TWIST1 gene or more rarely in the FGFR2 or FGFR3 genes. We have previously reported that patients with Saethre-Chotzen syndrome have an increased risk of developing breast cancer. Here we have analysed a cohort of 26 women with BRCA1/2-negative hereditary breast cancer to study whether a proportion of these families might have mutations in Saethre-Chotzen-associated genes. DNA sequence analysis of TWIST1 showed no pathogenic mutations in the coding sequence in any of the 26 patients. MLPA (multiplex ligation-dependent probe amplification)-analysis also showed no alterations in copy numbers in any of the craniofacial disorder genes MSX2, ALX4, RUNX2, EFNB1, TWIST1, FGFR1, FGFR2,FGFR3, or FGFR4. Taken together, our findings indicate that mutations in Saethre-Chotzen-associated genes are uncommon or absent in BRCA1/2-negative patients with hereditary breast cancer. AD - Lundberg Laboratory for Cancer Research, Department of Pathology, The Sahlgrenska Academy at the University of Gothenburg, Sahlgrenska University Hospital, Goteborg, Sweden. FAU - Bergman, Annika AU - Bergman A FAU - Sahlin, Pelle AU - Sahlin P FAU - Emanuelsson, Monica AU - Emanuelsson M FAU - Caren, Helena AU - Caren H FAU - Tarnow, Peter AU - Tarnow P FAU - Martinsson, Tommy AU - Martinsson T FAU - Gronberg, Henrik AU - Gronberg H FAU - Stenman, Goran AU - Stenman G LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Scand J Plast Reconstr Surg Hand Surg JT - Scandinavian journal of plastic and reconstructive surgery and hand surgery / Nordisk plastikkirurgisk forening [and] Nordisk klubb for handkirurgi JID - 8707869 RN - 0 (ALX4 protein, human) RN - 0 (Core Binding Factor Alpha 1 Subunit) RN - 0 (DNA-Binding Proteins) RN - 0 (EFNB1 protein, human) RN - 0 (Ephrin-B1) RN - 0 (Homeodomain Proteins) RN - 0 (MSX2 protein) RN - 0 (Nuclear Proteins) RN - 0 (RUNX2 protein, human) RN - 0 (TWIST1 protein, human) RN - 0 (Transcription Factors) RN - 0 (Twist Transcription Factor) RN - EC 2.7.1.112 (FGFR2 protein, human) RN - EC 2.7.1.112 (FGFR3 protein, human) RN - EC 2.7.1.112 (FGFR4 protein, human) RN - EC 2.7.10.1 (FGFR1 protein, human) RN - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1) RN - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2) RN - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 3) RN - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 4) SB - IM MH - Acrocephalosyndactylia/epidemiology/*genetics MH - Adult MH - Breast Neoplasms/epidemiology/genetics MH - Core Binding Factor Alpha 1 Subunit/genetics MH - DNA-Binding Proteins/genetics MH - Ephrin-B1/genetics MH - Female MH - Genes, BRCA1 MH - Genes, BRCA2 MH - *Genetic Testing MH - *Germ-Line Mutation MH - Homeodomain Proteins/genetics MH - Humans MH - Middle Aged MH - Nuclear Proteins/*genetics MH - Polymerase Chain Reaction MH - Receptor, Fibroblast Growth Factor, Type 1/genetics MH - Receptor, Fibroblast Growth Factor, Type 2/genetics MH - Receptor, Fibroblast Growth Factor, Type 3/*genetics MH - Receptor, Fibroblast Growth Factor, Type 4/genetics MH - Sequence Analysis, DNA MH - Transcription Factors/genetics MH - Twist Transcription Factor/*genetics EDAT- 2009/10/30 06:00 MHDA- 2010/11/17 06:00 CRDT- 2009/10/30 06:00 AID - 10.3109/02844310903247228 [pii] AID - 10.3109/02844310903247228 [doi] PST - ppublish SO - Scand J Plast Reconstr Surg Hand Surg. 2009;43(5):251-5. PMID- 19859804 OWN - NLM STAT- MEDLINE DA - 20100714 DCOM- 20101026 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 3 DP - 2010 Aug TI - Analysis of breast cancer related gene expression using natural splines and the Cox proportional hazard model to identify prognostic associations. PG - 711-20 AB - Many studies correlating gene expression data to clinical parameters assume a linear increase or decrease of the clinical parameter under investigation with the expression of a gene. We have studied genes encoding important breast cancer-related proteins using a model for survival-type data that is based on natural splines and the Cox proportional hazard model, thereby removing the linearity assumption. Expression data of 16 genes were studied in relation to metastasis-free probability in a cohort of 295 consecutive breast cancer patients treated at The Netherlands Cancer Institute. The independent predictive power for disease outcome of the 16 individual genes was tested in a multivariable model with known clinical and pathological risk factors. There is a linear relationship between increasing expression and a higher or lower hazard for distant metastasis for ESR1, ERBB4, VEGF, CCNE2, EZH2, and UPA; for ERBB2, ERBB3, CCND1, CCNE1, EED, CXCR4, CCR7, SDF1, and PAI1 there is no clear increase or decrease; and for EGFR there seems to be a non-linear relation. Multivariable analysis showed that the 70-gene prognosis profile outperforms all the other variables in the model (hazard-rate 5.4, 95% CI 2.5-11.7; P = 0.000018). EGFR-expression seems to have a non-linear relation with disease outcome, indicating that lower but also higher expression of EGFR are associated with worse outcome compared to intermediate expression levels; the other genes show no or a linear relation. AD - Division of Radiation Oncology, The Netherlands Cancer Institute, Plesmanlaan 121, Amsterdam 1066 CX, The Netherlands. FAU - Kreike, Bas AU - Kreike B FAU - Hart, Guus AU - Hart G FAU - Bartelink, Harry AU - Bartelink H FAU - van de Vijver, Marc J AU - van de Vijver MJ LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091027 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Tumor Markers, Biological) SB - IM MH - Breast Neoplasms/*diagnosis/*genetics/secondary MH - Cohort Studies MH - Female MH - *Gene Expression Profiling MH - Humans MH - Middle Aged MH - Netherlands MH - Oligonucleotide Array Sequence Analysis MH - Prognosis MH - *Proportional Hazards Models MH - Regression Analysis MH - Tumor Markers, Biological/*genetics EDAT- 2009/10/28 06:00 MHDA- 2010/10/27 06:00 CRDT- 2009/10/28 06:00 PHST- 2009/09/15 [received] PHST- 2009/10/08 [accepted] PHST- 2009/10/27 [aheadofprint] AID - 10.1007/s10549-009-0588-6 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Aug;122(3):711-20. Epub 2009 Oct 27. PMID- 19760033 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - The complete family of epidermal growth factor receptors and their ligands are co-ordinately expressed in breast cancer. PG - 105-10 AB - The levels of expression of the four receptors and eleven ligands composing the epidermal growth factor family were measured using immunohistochemical staining in one hundred cases of breast cancer. All of the family were expressed to some degree in some cases; however, individual cases showed a very wide range of expression of the family from essentially none to all the factors at high levels. The highest aggregate level of expression of a receptor was HER2 followed by HER1, then HER3, then HER4. The ligands (including two splice variants of the NRG1 and NRG2 genes) broadly fell into three groups, those with the highest aggregate expression were Epigen, Epiregulin, Neuregulin 1alpha, Neuregulin 2alpha, Neuregulin 2beta, Neuregulin 4 and TGFalpha, moderate expression was seen with EGF, Neuregulin 1beta and Neuregulin 3, and relatively low levels of expression were seen of HB-EGF, Betacellulin and Amphiregulin. Statistical analysis using Spearman's Rank Correlation showed a positive correlation of expression between each of the factors. Analysing the data using the Cox Proportional Hazards model showed that, in this dataset, the most powerful predictors of relapse free interval and overall survival were the combined measurement of only Epigen and Neuregulin 4. AD - Computing Laboratory, University of Kent, Canterbury, Kent CT1 7NJ, UK. FAU - McIntyre, Emmet AU - McIntyre E FAU - Blackburn, Edith AU - Blackburn E FAU - Brown, Philip J AU - Brown PJ FAU - Johnson, Colin G AU - Johnson CG FAU - Gullick, William J AU - Gullick WJ LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20090917 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (BTC protein, human) RN - 0 (Glycoproteins) RN - 0 (HER2 protein, human) RN - 0 (Intercellular Signaling Peptides and Proteins) RN - 0 (Ligands) RN - 0 (Neoplasm Proteins) RN - 0 (Neuregulins) RN - 0 (Receptors, Growth Factor) RN - 0 (Transforming Growth Factor alpha) RN - 0 (epigen) RN - 117147-70-3 (amphiregulin) RN - 62229-50-9 (Epidermal Growth Factor) RN - EC 2.7.1.112 (ERBB4 protein) RN - EC 2.7.10.1 (EGFR protein, human) RN - EC 2.7.10.1 (Receptor, Epidermal Growth Factor) RN - EC 2.7.10.1 (Receptor, erbB-2) RN - EC 2.7.10.1 (Receptor, erbB-3) SB - IM MH - Breast Neoplasms/*genetics/metabolism MH - Disease-Free Survival MH - Epidermal Growth Factor/biosynthesis/genetics MH - Female MH - Gene Expression Profiling MH - *Gene Expression Regulation, Neoplastic MH - Genes, erbB MH - Genes, erbB-1 MH - Genes, erbB-2 MH - Glycoproteins/biosynthesis/genetics MH - Humans MH - Intercellular Signaling Peptides and Proteins/biosynthesis/genetics MH - Ligands MH - *Multigene Family MH - Neoplasm Proteins/biosynthesis/*genetics MH - Neuregulins/biosynthesis/genetics MH - Prognosis MH - Proportional Hazards Models MH - Receptor, Epidermal Growth Factor/biosynthesis/genetics MH - Receptor, erbB-2/biosynthesis MH - Receptor, erbB-3/biosynthesis MH - Receptors, Growth Factor/biosynthesis/*genetics MH - Transforming Growth Factor alpha/biosynthesis/genetics EDAT- 2009/09/18 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/09/18 06:00 PHST- 2009/02/06 [received] PHST- 2009/08/27 [accepted] PHST- 2009/09/17 [aheadofprint] AID - 10.1007/s10549-009-0536-5 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):105-10. Epub 2009 Sep 17. PMID- 19754664 OWN - NLM STAT- MEDLINE DA - 20100726 DCOM- 20101028 IS - 1582-4934 (Electronic) IS - 1582-1838 (Linking) VI - 13 IP - 10 DP - 2009 Oct TI - Genetic characterization of breast cancer and implications for clinical management. PG - 4090-103 AB - Breast cancer is a genetic disease caused by the accumulation of mutations in neoplastic cells. In the last few years, high-throughput microarray-based molecular analysis has provided increasingly more coherent information about the genetic aberrations in breast cancer. New biomarkers and molecular techniques are slowly becoming part of the diagnostic and prognostic armamentarium available for pathologists and oncologists to tailor the therapy for breast cancer patients. In this review, we will focus on the contribution of breast cancer somatic genetics to our understanding of breast cancer biology and its impact on breast cancer patient management. AD - Molecular Pathology Laboratory, The Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK. FAU - Geyer, Felipe C AU - Geyer FC FAU - Lopez-Garcia, Maria A AU - Lopez-Garcia MA FAU - Lambros, Maryou B AU - Lambros MB FAU - Reis-Filho, Jorge S AU - Reis-Filho JS LA - eng PT - Journal Article PT - Review DEP - 20090914 PL - England TA - J Cell Mol Med JT - Journal of cellular and molecular medicine JID - 101083777 RN - 0 (Tumor Markers, Biological) SB - IM MH - Breast Neoplasms/*genetics/*therapy MH - Female MH - Gene Expression Regulation, Neoplastic MH - Genetic Association Studies MH - High-Throughput Screening Assays MH - Humans MH - *Individualized Medicine MH - Tumor Markers, Biological/metabolism EDAT- 2009/09/17 06:00 MHDA- 2010/10/29 06:00 CRDT- 2009/09/17 06:00 PHST- 2009/09/14 [aheadofprint] AID - JCMM906 [pii] AID - 10.1111/j.1582-4934.2009.00906.x [doi] PST - ppublish SO - J Cell Mol Med. 2009 Oct;13(10):4090-103. Epub 2009 Sep 14. PMID- 19728083 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - Evidence for a transcriptional signature of breast cancer. PG - 65-75 AB - Cancer arises from a step-wise accumulation of genetic and epigenetic changes in oncogenes and tumor suppressor genes, followed by changes in transcription and protein profiles. To identify the intrinsic transcriptional features of breast cancer and to explore in more detail the molecular basis of breast carcinogenesis, genes differentially expressed between cancers and their paired normal breast samples in nine breast cancer patients were screened using microarray. Nine normal breast tissues and 49 breast cancer tissue samples were then clustered based on the set of differentially expressed genes. A transcriptional signature of breast cancer consisting of 188 differentially expressed genes was identified. This signature allowed the normal breast tissues to be distinguished from all of the breast cancer samples, and primary breast cancers could be classified into two phenotype-associated subgroups with different ER status and clinical outcome. Furthermore, the classification accuracy of the set of differentially expressed genes was validated in publically available breast microarray data. Moreover, the differentially expressed genes could be grouped into five subclusters involved in different biological processes of carcinogenesis. Most genes in a given subcluster interacted within an independent subnetwork, and subnetworks could cross-talk through a set of signal molecules. Thus, the transcriptional signature identified here may be an intrinsic feature of breast cancer, and it may constitute to the molecular basis of breast carcinogenesis and different phenotypes of breast cancer. AD - School of Pharmaceutical Science and Technology, Tianjin University, 300072 Tianjin, China. FAU - Feng, Yumei AU - Feng Y FAU - Li, Xiaoqing AU - Li X FAU - Sun, Baocun AU - Sun B FAU - Wang, Yuli AU - Wang Y FAU - Zhang, Lina AU - Zhang L FAU - Pan, Xiuhua AU - Pan X FAU - Chen, Xiaohui AU - Chen X FAU - Wang, Xiaoyan AU - Wang X FAU - Wang, Jinfeng AU - Wang J FAU - Hao, Xishan AU - Hao X LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20090902 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (Estrogens) RN - 0 (Neoplasm Proteins) RN - 0 (RNA, Messenger) RN - 0 (RNA, Neoplasm) SB - IM MH - Breast/metabolism MH - Breast Neoplasms/*genetics/metabolism/mortality MH - Carcinoma, Ductal, Breast/*genetics/metabolism/mortality/secondary MH - Computer Systems MH - Estrogens MH - Female MH - *Gene Expression Profiling MH - Gene Expression Regulation, Neoplastic/*genetics MH - Gene Regulatory Networks MH - Genes, Neoplasm MH - Humans MH - Kaplan-Meiers Estimate MH - Lymphatic Metastasis MH - Neoplasm Proteins/biosynthesis/*genetics MH - Neoplasms, Hormone-Dependent/genetics/metabolism/mortality/secondary MH - Oligonucleotide Array Sequence Analysis MH - RNA, Messenger/biosynthesis MH - RNA, Neoplasm/biosynthesis MH - Reverse Transcriptase Polymerase Chain Reaction MH - Subtraction Technique MH - *Transcription, Genetic EDAT- 2009/09/04 06:00 MHDA- 2010/10/26 06:00 CRDT- 2009/09/04 06:00 PHST- 2009/04/05 [received] PHST- 2009/08/06 [accepted] PHST- 2009/09/02 [aheadofprint] AID - 10.1007/s10549-009-0505-z [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):65-75. Epub 2009 Sep 2. PMID- 19701705 OWN - NLM STAT- MEDLINE DA - 20100610 DCOM- 20101025 IS - 1573-7217 (Electronic) IS - 0167-6806 (Linking) VI - 122 IP - 1 DP - 2010 Jul TI - PIK3CA expression in invasive breast cancer: a biomarker of poor prognosis. PG - 45-53 AB - The implications of Phosphatidylinositol 3-kinase (PIK3CA) mutations and its aberrant protein expression in breast cancer (BC) different molecular subtypes and patients' outcome remain controversial. The aims of this study were to assess the prevalence and clinical significance of PIK3CA protein expression in BC and to determine its association with its different molecular classes. PIK3CA protein expression was assessed in a well-characterized series of early stage BC (n = 1,394) with long-term follow-up, using tissue microarrays and immunohistochemistry. Associations between PIK3CA expression and clinicopathological variables, molecular classes, and patients' outcome were investigated. Positive PIK3CA expression was associated with poor prognostic variables including higher grade, larger size, nodal involvement, vascular invasion, and higher proliferative fraction (P < 0.001). Increased PIK3CA expression was associated with the basal-like breast cancer (BLBC) and HER2-positive classes as well as triple negative non-basal (TNnon-B) tumors (P < 0.001). The luminal class showed reduced PIK3CA expression relative to other classes. Patients with PIK3CA positive tumors had shorter BC specific and disease free survival, independent of other prognostic factors except grade. Similar associations with outcome were found when the analysis was restricted to the large luminal class of tumors. PIK3CA is an oncogenic biomarker associated with poor prognosis in BC. Although, PIK3CA over-expression was more prevalent in BLBC and HER2-positive tumors it appeared to be a marker of poor differentiation rather than of a particular subtype. Thus, targeting of PIK3CA using specific inhibitors could potentially be beneficial, particularly for patients with more aggressive poorly differentiated tumors, irrespective of their molecular subtype. AD - Division of Pathology, School of Molecular Medical Sciences, University of Nottingham, Queen's Medical Centre, Clifton Boulevard, Nottingham NG7 2UH, UK. FAU - Aleskandarany, Mohammed A AU - Aleskandarany MA FAU - Rakha, Emad A AU - Rakha EA FAU - Ahmed, Mohamed A H AU - Ahmed MA FAU - Powe, Desmond G AU - Powe DG FAU - Paish, Emma C AU - Paish EC FAU - Macmillan, R Douglas AU - Macmillan RD FAU - Ellis, Ian O AU - Ellis IO FAU - Green, Andrew R AU - Green AR LA - eng PT - Journal Article DEP - 20090822 PL - Netherlands TA - Breast Cancer Res Treat JT - Breast cancer research and treatment JID - 8111104 RN - 0 (HER2 protein, human) RN - 0 (Neoplasm Proteins) RN - 0 (Receptors, Steroid) RN - 0 (Tumor Markers, Biological) RN - EC 2.7.1.137 (1-Phosphatidylinositol 3-Kinase) RN - EC 2.7.1.137 (PIK3CA protein, human) RN - EC 2.7.10.1 (Receptor, erbB-2) SB - IM MH - 1-Phosphatidylinositol 3-Kinase/*analysis/biosynthesis/genetics MH - Breast Neoplasms/enzymology/*genetics/mortality/pathology MH - Carcinoma/enzymology/*genetics/mortality/pathology MH - Disease-Free Survival MH - Female MH - Follow-Up Studies MH - Gene Expression Profiling MH - Gene Expression Regulation, Neoplastic MH - Humans MH - Immunoenzyme Techniques MH - Kaplan-Meiers Estimate MH - Neoplasm Invasiveness MH - Neoplasm Proteins/*analysis/biosynthesis/genetics MH - Oligonucleotide Array Sequence Analysis MH - Prognosis MH - Proportional Hazards Models MH - Receptor, erbB-2/analysis MH - Receptors, Steroid/analysis MH - Tumor Markers, Biological/*analysis EDAT- 2009/08/25 09:00 MHDA- 2010/10/26 06:00 CRDT- 2009/08/25 09:00 PHST- 2009/08/04 [received] PHST- 2009/08/06 [accepted] PHST- 2009/08/22 [aheadofprint] AID - 10.1007/s10549-009-0508-9 [doi] PST - ppublish SO - Breast Cancer Res Treat. 2010 Jul;122(1):45-53. Epub 2009 Aug 22. PMID- 19659662 OWN - NLM STAT- MEDLINE DA - 20100607 DCOM- 20101029 IS - 1365-2354 (Electronic) IS - 0961-5423 (Linking) VI - 19 IP - 3 DP - 2010 May TI - BRCA testing of breast cancer patients: medical specialists' referral patterns, knowledge and attitudes to genetic testing. PG - 369-76 AB - This study explores knowledge about hereditary breast cancer, attitudes about BRCA testing and referral pattern to a family cancer clinic among medical specialists. A total of 92 questionnaires were completed by surgeons (38), medical oncologists (29), radiation oncologists (13) and radiologists (12). The response rate was 51%. A substantial (11-56%) proportion of medical specialists do not refer patients who meet current criteria for BRCA testing. Although questions on inheritance were less well answered, overall knowledge was good. They had a positive attitude, but were concerned about the distress DNA testing might cause to family members. The majority (75%) stated that the best time for referral is after adjuvant therapy or during follow-up, but another important determinant was the patient's wish or need (12%). Further studies are needed to gain insight into the actual referral process, while ongoing training of medical specialists about genetic aspects of breast cancer is also necessary. AD - Department of Medical Genetics, University Medical Centre Utrecht, Utrecht, the Netherlands. e.vanriel@umcutrecht.nl FAU - Van Riel, E AU - Van Riel E FAU - Warlam-Rodenhuis, C C AU - Warlam-Rodenhuis CC FAU - Verhoef, S AU - Verhoef S FAU - Rutgers, E J T H AU - Rutgers EJ FAU - Ausems, M G E M AU - Ausems MG LA - eng PT - Journal Article DEP - 20090729 PL - England TA - Eur J Cancer Care (Engl) JT - European journal of cancer care JID - 9301979 SB - N MH - Adult MH - Aged MH - Attitude of Health Personnel MH - Breast Neoplasms/*diagnosis/*genetics MH - Female MH - *Genes, BRCA1 MH - Genes, BRCA2 MH - Genetic Counseling MH - Genetic Testing/*methods MH - Health Knowledge, Attitudes, Practice MH - Humans MH - Male MH - Middle Aged MH - Netherlands MH - *Physician's Practice Patterns MH - Questionnaires MH - Referral and Consultation/*statistics & numerical data EDAT- 2009/08/08 09:00 MHDA- 2010/10/30 06:00 CRDT- 2009/08/08 09:00 PHST- 2009/07/29 [aheadofprint] AID - ECC1065 [pii] AID - 10.1111/j.1365-2354.2008.01065.x [doi] PST - ppublish SO - Eur J Cancer Care (Engl). 2010 May;19(3):369-76. Epub 2009 Jul 29. PMID- 19629691 OWN - NLM STAT- MEDLINE DA - 20100715 DCOM- 20101108 IS - 1557-1920 (Electronic) IS - 1557-1912 (Linking) VI - 12 IP - 4 DP - 2010 Aug TI - Factors associated with breast cancer screening in Asian Indian women in metro-Detroit. PG - 534-43 AB - Few studies have examined social factors related to breast cancer screening in Asian Indian women in the Midwestern US. This cross-sectional, community-based survey utilized constructs of the Health Belief Model to examine factors associated with breast cancer screening among Asian Indian women in metropolitan Detroit, Michigan. Of the 160 participants, 63.8% reported receiving both a clinical breast exam and mammogram within the past 2 years. Women were more likely to screen for breast cancer if they had a college education, lived in the US for more years, perceived that breast cancer screening is useful in detecting breast cancer early, agreed that mammography was important, and received a recommendation by a healthcare provider to get a mammogram. These findings highlight the need for further research on regional differences in breast cancer screening knowledge, behaviors and predictors among Asian Pacific Islanders subgroups such as Asian Indian women who recently immigrated to the US. AD - Department of Health Behavior and Health Education, University of Michigan School of Public Health, 109 Observatory St, Ann Arbor, MI 48109, USA. FAU - Boxwala, Fatema I AU - Boxwala FI FAU - Bridgemohan, Areeta AU - Bridgemohan A FAU - Griffith, Derek M AU - Griffith DM FAU - Soliman, Amr S AU - Soliman AS LA - eng PT - Journal Article PL - United States TA - J Immigr Minor Health JT - Journal of immigrant and minority health / Center for Minority Public Health JID - 101256527 SB - IM MH - Adult MH - Asian Americans MH - Breast Neoplasms/diagnosis/ethnology/*prevention & control MH - Cross-Sectional Studies MH - Female MH - Humans MH - India/ethnology MH - Mass Screening/*utilization MH - Michigan MH - Middle Aged MH - *Patient Acceptance of Health Care MH - Questionnaires MH - Urban Population EDAT- 2009/07/25 09:00 MHDA- 2010/11/09 06:00 CRDT- 2009/07/25 09:00 AID - 10.1007/s10903-009-9277-0 [doi] PST - ppublish SO - J Immigr Minor Health. 2010 Aug;12(4):534-43. PMID- 19448619 OWN - NLM STAT- MEDLINE DA - 20100920 DCOM- 20101104 IS - 1546-1718 (Electronic) IS - 1061-4036 (Linking) VI - 41 IP - 6 DP - 2009 Jun TI - Loci at chromosomes 13, 19 and 20 influence age at natural menopause. PG - 645-7 AB - We conducted a genome-wide association study for age at natural menopause in 2,979 European women and identified six SNPs in three loci associated with age at natural menopause: chromosome 19q13.4 (rs1172822; -0.4 year per T allele (39%); P = 6.3 x 10(-11)), chromosome 20p12.3 (rs236114; +0.5 year per A allele (21%); P = 9.7 x 10(-11)) and chromosome 13q34 (rs7333181; +0.5 year per A allele (12%); P = 2.5 x 10(-8)). These common genetic variants regulate timing of ovarian aging, an important risk factor for breast cancer, osteoporosis and cardiovascular disease. AD - Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands. FAU - Stolk, Lisette AU - Stolk L FAU - Zhai, Guangju AU - Zhai G FAU - van Meurs, Joyce B J AU - van Meurs JB FAU - Verbiest, Michael M P J AU - Verbiest MM FAU - Visser, Jenny A AU - Visser JA FAU - Estrada, Karol AU - Estrada K FAU - Rivadeneira, Fernando AU - Rivadeneira F FAU - Williams, Frances M AU - Williams FM FAU - Cherkas, Lynn AU - Cherkas L FAU - Deloukas, Panos AU - Deloukas P FAU - Soranzo, Nicole AU - Soranzo N FAU - de Keyzer, Jules J AU - de Keyzer JJ FAU - Pop, Victor J M AU - Pop VJ FAU - Lips, Paul AU - Lips P FAU - Lebrun, Corinne E I AU - Lebrun CE FAU - van der Schouw, Yvonne T AU - van der Schouw YT FAU - Grobbee, Diederick E AU - Grobbee DE FAU - Witteman, Jacqueline AU - Witteman J FAU - Hofman, Albert AU - Hofman A FAU - Pols, Huibert A P AU - Pols HA FAU - Laven, Joop S E AU - Laven JS FAU - Spector, Tim D AU - Spector TD FAU - Uitterlinden, Andre G AU - Uitterlinden AG LA - eng GR - Wellcome Trust/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20090517 PL - United States TA - Nat Genet JT - Nature genetics JID - 9216904 SB - IM CIN - Nat Genet. 2009 Jun;41(6):637-8. PMID: 19471299 MH - Age Factors MH - Breast Neoplasms/genetics MH - Cardiovascular Diseases/genetics MH - Chromosomes, Human, Pair 13/*genetics MH - Chromosomes, Human, Pair 19/*genetics MH - Chromosomes, Human, Pair 20/*genetics MH - European Continental Ancestry Group/genetics MH - Female MH - Genetic Variation MH - *Genome-Wide Association Study MH - Humans MH - Menopause/*genetics MH - Meta-Analysis as Topic MH - Middle Aged MH - Odds Ratio MH - Osteoporosis/genetics MH - Polymorphism, Single Nucleotide MH - Risk Factors MH - Twin Studies as Topic EDAT- 2009/05/19 09:00 MHDA- 2010/11/05 06:00 CRDT- 2009/05/19 09:00 PHST- 2008/09/04 [received] PHST- 2009/04/21 [accepted] PHST- 2009/05/17 [aheadofprint] AID - ng.387 [pii] AID - 10.1038/ng.387 [doi] PST - ppublish SO - Nat Genet. 2009 Jun;41(6):645-7. Epub 2009 May 17. PMID- 19346409 OWN - NLM STAT- MEDLINE DA - 20100524 DCOM- 20101026 IS - 1524-8399 (Print) IS - 1524-8399 (Linking) VI - 11 IP - 3 DP - 2010 May TI - Considering organizational factors in addressing health care disparities: two case examples. PG - 367-76 AB - Policy makers and practitioners have yet to successfully understand and eliminate persistent racial differences in health care quality. Interventions to address these racial health care disparities have largely focused on increasing cultural awareness and sensitivity, promoting culturally competent care, and increasing providers' adherence to evidence-based guidelines. Although these strategies have improved some proximal factors associated with service provision, they have not had a strong impact on racial health care disparities. Interventions to date have had limited impact on racial differences in health care quality, in part, because they have not adequately considered or addressed organizational and institutional factors. In this article, we describe an emerging intervention strategy to reduce health care disparities called dismantling (undoing) racism and how it has been adapted to a rural public health department and an urban medical system. These examples illustrate the importance of adapting interventions to the organizational and institutional context and have important implications for practitioners and policy makers. AD - University of Michigan School of Public Health in Ann Arbor, Michigan, USA. derekmg@umich.edu FAU - Griffith, Derek M AU - Griffith DM FAU - Yonas, Michael AU - Yonas M FAU - Mason, Mondi AU - Mason M FAU - Havens, Betsy E AU - Havens BE LA - eng PT - Journal Article DEP - 20090403 PL - United States TA - Health Promot Pract JT - Health promotion practice JID - 100890609 SB - IM MH - Breast Neoplasms/ethnology MH - Delivery of Health Care MH - Female MH - Health Promotion/*methods/*organization & administration MH - Healthcare Disparities/*organization & administration MH - Humans MH - Male MH - Organizational Case Studies MH - Organizational Culture MH - Organizational Innovation MH - *Prejudice MH - Program Evaluation MH - Public Health Administration MH - Quality of Health Care/*organization & administration MH - Rural Health Services MH - Southeastern United States MH - Urban Health Services EDAT- 2009/04/07 09:00 MHDA- 2010/10/27 06:00 CRDT- 2009/04/07 09:00 PHST- 2009/04/03 [aheadofprint] AID - 1524839908330863 [pii] AID - 10.1177/1524839908330863 [doi] PST - ppublish SO - Health Promot Pract. 2010 May;11(3):367-76. Epub 2009 Apr 3.