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231

Nature genetics. 2014:46(9):994-1000.DOI: 10.1038/ng.3052

Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer

Wolpin, Brian M; Rizzato, Cosmeri; Kraft, Peter; Kooperberg, Charles; Petersen, Gloria M; Wang, Zhaoming; Arslan, Alan A; Beane-Freeman, Laura; Bracci, Paige M; Buring, Julie; Canzian, Federico; Duell, Eric J; Gallinger, Steven; Giles, Graham G; Goodman, Gary E; Goodman, Phyllis J; Jacobs, Eric J; Kamineni, Aruna; Klein, Alison P; Kolonel, Laurence N; Kulke, Matthew H; Li, Donghui; Malats, Nuria; Olson, Sara H; Risch, Harvey A; Sesso, Howard D; Visvanathan, Kala; White, Emily; Zheng, Wei; Abnet, Christian C; Albanes, Demetrius; Andreotti, Gabriella; Austin, Melissa A; Barfield, Richard; Basso, Daniela; Berndt, Sonja I; Boutron-Ruault, Marie-Christine; Brotzman, Michelle; Buchler, Markus W; Bueno-de-Mesquita, H Bas; Bugert, Peter; Burdette, Laurie; Campa, Daniele; Caporaso, Neil E; Capurso, Gabriele; Chung, Charles; Cotterchio, Michelle; Costello, Eithne; Elena, Joanne; Funel, Niccola; Gaziano, J Michael; Giese, Nathalia A; Giovannucci, Edward L; Goggins, Michael; Gorman, Megan J; Gross, Myron; Haiman, Christopher A; Hassan, Manal; Helzlsouer, Kathy J; Henderson, Brian E; Holly, Elizabeth A; Hu, Nan; Hunter, David J; Innocenti, Federico; Jenab, Mazda; Kaaks, Rudolf; Key, Timothy J; Khaw, Kay-Tee; Klein, Eric A; Kogevinas, Manolis; Krogh, Vittorio; Kupcinskas, Juozas; Kurtz, Robert C; LaCroix, Andrea; Landi, Maria T; Landi, Stefano; Le Marchand, Loic; Mambrini, Andrea; Mannisto, Satu; Milne, Roger L; Nakamura, Yusuke; Oberg, Ann L; Owzar, Kouros; Patel, Alpa V; Peeters, Petra H M; Peters, Ulrike; Pezzilli, Raffaele; Piepoli, Ada; Porta, Miquel; Real, Francisco X; Riboli, Elio; Rothman, Nathaniel; Scarpa, Aldo; Shu, Xiao-Ou; Silverman, Debra T; Soucek, Pavel; Sund, Malin; Talar-Wojnarowska, Renata; Taylor, Philip R; Theodoropoulos, George E; Thornquist, Mark; Tjonneland, Anne; Tobias, Geoffrey S; Trichopoulos, Dimitrios; Vodicka, Pavel; Wactawski-Wende, Jean; Wentzensen, Nicolas; Wu, Chen; Yu, Herbert; Yu, Kai; Zeleniuch-Jacquotte, Anne; Hoover, Robert; Hartge, Patricia; Fuchs, Charles; Chanock, Stephen J; Stolzenberg-Solomon, Rachael S; Amundadottir, Laufey T
We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 x 10-12), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 x 10-10), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 x 10-9) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 x 10-8). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 x 10-14). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 x 10-7) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.
PMCID:4191666
PMID: 25086665
ISSN: 1061-4036
CID: 1105052
Cancer epidemiology biomarkers & prevention. 2014:23(7):1290-7.DOI: 10.1158/1055-9965.EPI-14-0009

Circulating Estrogen Metabolites and Risk of Breast Cancer in Postmenopausal Women

Arslan, Alan A; Koenig, Karen L; Lenner, Per; Afanasyeva, Yelena; Shore, Roy E; Chen, Yu; Lundin, Eva; Toniolo, Paolo; Hallmans, Goran; Zeleniuch-Jacquotte, Anne
Background: It has been hypothesized that predominance of the 2-hydroxylation estrogen metabolism pathway over the 16alpha-hydroxylation pathway may be inversely associated with breast cancer risk. Methods: We examined the associations of invasive breast cancer risk with circulating 2-OHE1, 16alpha-OHE1, and the 2-OHE1:16alpha-OHE1 ratio in a case-control study of postmenopausal women nested within two prospective cohorts: the New York University Women's Health Study (NYUWHS) and the Northern Sweden Mammary Screening Cohort (NSMSC), with adjustment for circulating levels of estrone, and additional analyses by tumor estrogen receptor (ER) status. Levels of 2-OHE1 and 16alpha-OHE1 were measured using ESTRAMET 2/16 assay in stored serum or plasma samples from 499 incident breast cancer cases and 499 controls, who were matched on cohort, age, and date of blood donation. Results: Overall, no significant associations were observed between breast cancer risk and circulating levels of 2-OHE1, 16alpha-OHE1, or their ratio in either cohort and in combined analyses. For 2-OHE1, there was evidence of heterogeneity by ER status in models adjusting for estrone (p
PMCID:4082442
PMID: 24769889
ISSN: 1055-9965
CID: 922822
Cancer epidemiology biomarkers & prevention. 2014:23(6):1121-4.DOI: 10.1158/1055-9965.EPI-13-0627

Variants Associated with Susceptibility to Pancreatic Cancer and Melanoma Do Not Reciprocally Affect Risk

Wu, Lang; Goldstein, Alisa M; Yu, Kai; Yang, Xiaohong R; Rabe, Kari G; Arslan, Alan A; Canzian, Federico; Wolpin, Brian M; Stolzenberg-Solomon, Rachael; Amundadottir, Laufey T; Petersen, Gloria M
Background: Melanoma cases may exist in pancreatic cancer kindreds, while there is increased risk of pancreatic cancer in familial melanoma. The two cancers may share genetic susceptibility variants in common. Methods: Three dbGaP-deposited GWAS datasets (MD Anderson melanoma, PanScan 1, and PanScan 2 for pancreatic cancer) were used. Thirty-seven melanoma susceptibility variants in 22 genomic regions from published GWAS, plus melanoma-related genes and pathways were examined for pancreatic cancer risk in the PanScan datasets. Conversely, nine known pancreatic cancer susceptibility variants were examined for melanoma risk in the MD Anderson dataset. Results: In the PanScan data, initial associations were found with melanoma susceptibility variants in NCOA6 (rs4911442) (OR=1.32, 95% CI 1.03-1.70, p=0.03), YWHAZP5 (rs17119461) (OR=2.62, 95% CI 1.08-6.35, p=0.03), and YWHAZP5 (rs17119490) (OR=2.62, 95% CI 1.08-6.34, p=0.03), TYRP1 (p=0.04), and IFNA13 (p=0.04). In the melanoma dataset, two pancreatic cancer susceptibility variants were associated: NR5A2 (rs12029406) (OR=1.39, 95% CI 1.01-1.92, p=0.04) and CLPTM1L-TERT (rs401681) (OR=1.16, 95% CI 1.01-1.34, p=0.04). None of these associations remained significant after correcting for multiple comparisons. Conclusion: Reported variants of melanoma genes and pathways do not play a role in pancreatic cancer predisposition. Reciprocally, pancreatic cancer susceptibility variants are not associated with melanoma risk. Impact: Known melanoma-related genes and pathways, as well as GWAS-derived susceptibility variants of melanoma and pancreatic cancer, do not explain the shared genetic etiology of these two cancers.
PMCID:4120837
PMID: 24642353
ISSN: 1055-9965
CID: 951172
Ultrasound in obstetrics & gynecology. 2014:43(4):383-95.DOI: 10.1002/uog.13282

Cesarean scar pregnancy and early placenta accreta share common histology

Timor-Tritsch, I E; Monteagudo, A; Cali, G; Palacios-Jaraquemada, J M; Maymon, R; Arslan, A A; Patil, N; Popiolek, D; Mittal, K R
OBJECTIVE: To determine, by evaluation of histological slides, images and descriptions of early (second-trimester) placenta accreta (EPA) and placental implantation in cases of Cesarean scar pregnancy (CSP), whether these are pathologically indistinguishable and whether they both represent different stages in the disease continuum leading to morbidly adherent placenta in the third trimester. METHODS: The database of a previously published review of CSP and EPA was used to identify articles with histopathological descriptions and electronic images for pathological review. When possible, microscopic slides and/or paraffin blocks were obtained from the original researchers. We also included from our own institutions cases of CSP and EPA for which pathology specimens were available. Two pathologists examined all the material independently and, blinded to each other's findings, provided a pathological diagnosis based on microscopic appearance. Interobserver agreement in diagnosis was determined. RESULTS: Forty articles were identified, which included 31 cases of CSP and 13 cases of EPA containing histopathological descriptions and/or images of the pathology. We additionally included six cases of CSP and eight cases of EPA from our own institutions, giving a total of 58 cases available for histological evaluation (37 CSP and 21 EPA) containing clear definitions of morbidly adherent placenta. In the 29 cases for which images/slides were available for histopathological evaluation, both pathologists attested to the various degrees of myometrial and/or scar tissue invasion by placental villi with scant or no intervening decidua, consistent with the classic definition of morbidly adherent placenta. Based on the reviewed material, cases with a diagnosis of EPA and those with a diagnosis of CSP showed identical histopathological features. Interobserver correlation was high (kappa = 0.93). CONCLUSIONS: EPA and placental implantation in CSP are histopathologically indistinguishable and may represent different stages in the disease continuum leading to morbidly adherent placenta in the third trimester
PMID: 24357257
ISSN: 0960-7692
CID: 953052
Gut. 2014:63(1):152-60.DOI: 10.1136/gutjnl-2012-303477

Genome-wide association study of survival in patients with pancreatic adenocarcinoma

Wu, Chen; Kraft, Peter; Stolzenberg-Solomon, Rachael; Steplowski, Emily; Brotzman, Michelle; Xu, Mousheng; Mudgal, Poorva; Amundadottir, Laufey; Arslan, Alan A; Bueno-de-Mesquita, H Bas; Gross, Myron; Helzlsouer, Kathy; Jacobs, Eric J; Kooperberg, Charles; Petersen, Gloria M; Zheng, Wei; Albanes, Demetrius; Boutron-Ruault, Marie-Christine; Buring, Julie E; Canzian, Federico; Cao, Guangwen; Duell, Eric J; Elena, Joanne W; Gaziano, J Michael; Giovannucci, Edward L; Hallmans, Goran; Hutchinson, Amy; Hunter, David J; Jenab, Mazda; Jiang, Guoliang; Khaw, Kay-Tee; Lacroix, Andrea; Li, Zhaoshen; Mendelsohn, Julie B; Panico, Salvatore; Patel, Alpa V; Qian, Zhi Rong; Riboli, Elio; Sesso, Howard; Shen, Hongbing; Shu, Xiao-Ou; Tjonneland, Anne; Tobias, Geoffrey S; Trichopoulos, Dimitrios; Virtamo, Jarmo; Visvanathan, Kala; Wactawski-Wende, Jean; Wang, Chengfeng; Yu, Kai; Zeleniuch-Jacquotte, Anne; Chanock, Stephen; Hoover, Robert; Hartge, Patricia; Fuchs, Charles S; Lin, Dongxin; Wolpin, Brian M
BACKGROUND AND OBJECTIVE: Survival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma. METHODS: We analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p
PMCID:3816124
PMID: 23180869
ISSN: 0017-5749
CID: 222822
Cancer causes & control. ccc. 2013:24(4):741-8.DOI: 10.1007/s10552-013-0156-6

Circulating prolactin levels and risk of epithelial ovarian cancer

Clendenen, Tess V; Arslan, Alan A; Lokshin, Anna E; Liu, Mengling; Lundin, Eva; Koenig, Karen L; Berrino, Franco; Hallmans, Goran; Idahl, Annika; Krogh, Vittorio; Lukanova, Annekatrin; Marrangoni, Adele; Muti, Paola; Nolen, Brian M; Ohlson, Nina; Shore, Roy E; Sieri, Sabina; Zeleniuch-Jacquotte, Anne
PURPOSE: Indirect evidence from experimental and epidemiological studies suggests that prolactin may be involved in ovarian cancer development. However, the relationship between circulating prolactin levels and risk of ovarian cancer is unknown. METHODS: We conducted a nested case-control study of 230 cases and 432 individually matched controls within three prospective cohorts to evaluate whether pre-diagnostic circulating prolactin is associated with subsequent risk of ovarian cancer. We also assessed whether lifestyle and reproductive factors are associated with circulating prolactin among controls. RESULTS: Prolactin levels were significantly lower among post- versus pre-menopausal women, parous versus nulliparous women, and past versus never users of oral contraceptives in our cross-sectional analysis of controls. In our nested case-control study, we observed a non-significant positive association between circulating prolactin and ovarian cancer risk (OR(Q4vsQ1) 1.56, 95 % CI 0.94, 2.63, p trend 0.15). Our findings were similar in multivariate-adjusted models and in the subgroup of women who donated blood >/=5 years prior to diagnosis. We observed a significant positive association between prolactin and risk for the subgroup of women with BMI >/=25 kg/m(2) (OR(Q4vsQ1) 3.10, 95 % CI 1.39, 6.90), but not for women with BMI <25 kg/m(2) (OR(Q4vsQ1) 0.81, 95 % CI 0.40, 1.64). CONCLUSIONS: Our findings suggest that prolactin may be associated with increased risk of ovarian cancer, particularly in overweight/obese women. Factors associated with reduced risk of ovarian cancer, such as parity and use of oral contraceptives, were associated with lower prolactin levels, which suggests that modulation of prolactin may be a mechanism underlying their association with risk.
PMCID:3602319
PMID: 23378139
ISSN: 0957-5243
CID: 222782
Cancer causes & control. ccc. 2013:24(3):595-602.DOI: 10.1007/s10552-012-0138-0

Polymorphisms in genes related to one-carbon metabolism are not related to pancreatic cancer in PanScan and PanC4

Leenders, Max; Bhattacharjee, Samsiddhi; Vineis, Paolo; Stevens, Victoria; Bueno-de-Mesquita, H Bas; Shu, Xiao-Ou; Amundadottir, Laufey; Gross, Myron; Tobias, Geoffrey S; Wactawski-Wende, Jean; Arslan, Alan A; Duell, Eric J; Fuchs, Charles S; Gallinger, Steven; Hartge, Patricia; Hoover, Robert N; Holly, Elizabeth A; Jacobs, Eric J; Klein, Alison P; Kooperberg, Charles; Lacroix, Andrea; Li, Donghui; Mandelson, Margaret T; Olson, Sara H; Petersen, Gloria; Risch, Harvey A; Yu, Kai; Wolpin, Brian M; Zheng, Wei; Agalliu, Ilir; Albanes, Demetrius; Boutron-Ruault, Marie-Christine; Bracci, Paige M; Buring, Julie E; Canzian, Federico; Chang, Kenneth; Chanock, Stephen J; Cotterchio, Michelle; Gaziano, J Michael; Giovanucci, Edward L; Goggins, Michael; Hallmans, Goran; Hankinson, Susan E; Hoffman-Bolton, Judith A; Hunter, David J; Hutchinson, Amy; Jacobs, Kevin B; Jenab, Mazda; Khaw, Kay-Tee; Kraft, Peter; Krogh, Vittorio; Kurtz, Robert C; McWilliams, Robert R; Mendelsohn, Julie B; Patel, Alpa V; Rabe, Kari G; Riboli, Elio; Tjonneland, Anne; Trichopoulos, Dimitrios; Virtamo, Jarmo; Visvanathan, Kala; Elena, Joanne W; Yu, Herbert; Zeleniuch-Jacquotte, Anne; Stolzenberg-Solomon, Rachael Z
PURPOSE: The evidence of a relation between folate intake and one-carbon metabolism (OCM) with pancreatic cancer (PanCa) is inconsistent. In this study, the association between genes and single-nucleotide polymorphisms (SNPs) related to OCM and PanCa was assessed. METHODS: Using biochemical knowledge of the OCM pathway, we identified thirty-seven genes and 834 SNPs to examine in association with PanCa. Our study included 1,408 cases and 1,463 controls nested within twelve cohorts (PanScan). The ten SNPs and five genes with lowest p values (<0.02) were followed up in 2,323 cases and 2,340 controls from eight case-control studies (PanC4) that participated in PanScan2. The correlation of SNPs with metabolite levels was assessed for 649 controls from the European Prospective Investigation into Cancer and Nutrition. RESULTS: When both stages were combined, we observed suggestive associations with PanCa for rs10887710 (MAT1A) (OR 1.13, 95 %CI 1.04-1.23), rs1552462 (SYT9) (OR 1.27, 95 %CI 1.02-1.59), and rs7074891 (CUBN) (OR 1.91, 95 %CI 1.12-3.26). After correcting for multiple comparisons, no significant associations were observed in either the first or second stage. The three suggested SNPs showed no correlations with one-carbon biomarkers. CONCLUSIONS: This is the largest genetic study to date to examine the relation between germline variations in OCM-related genes polymorphisms and the risk of PanCa. Suggestive evidence for an association between polymorphisms and PanCa was observed among the cohort-nested studies, but this did not replicate in the case-control studies. Our results do not strongly support the hypothesis that genes related to OCM play a role in pancreatic carcinogenesis.
PMCID:4127987
PMID: 23334854
ISSN: 0957-5243
CID: 222802
Breast cancer research. 2013:15(1).DOI: 10.1186/bcr3390

Circulating levels of 25-hydroxyvitamin D and risk of breast cancer: a nested case-control study

Scarmo, Stephanie; Afanasyeva, Yelena; Lenner, Per; Koenig, Karen L; Horst, Ronald L; Clendenen, Tess V; Arslan, Alan A; Chen, Yu; Hallmans, Goran; Lundin, Eva; Rinaldi, Sabina; Toniolo, Paolo; Shore, Roy E; Zeleniuch-Jacquotte, Anne
INTRODUCTION: Experimental evidence suggests a protective role for circulating 25-hydroxyvitamin D (25(OH)D) in breast cancer development, but the results of epidemiological studies have been inconsistent. METHODS: We conducted a case-control study nested within two prospective cohorts, the New York University Women's Health Study and the Northern Sweden Mammary Screening Cohort. Blood samples were collected at enrollment, and women were followed up for breast cancer ascertainment. In total, 1,585 incident breast cancer cases were individually-matched to 2,940 controls. Of these subjects, 678 cases and 1,208 controls contributed two repeat blood samples, at least one year apart. Circulating levels of 25(OH)D were measured, and multivariate odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. RESULTS: No association was observed between circulating levels of 25(OH)D and overall breast cancer risk (multivariate-adjusted model OR = 0.94, 95% CI = 0.76-1.16 for the highest vs. lowest quintile, ptrend = 0.30). The temporal reliability of 25(OH)D measured in repeat blood samples was high (intraclass correlation coefficients for season-adjusted 25(OH)D > 0.70). An inverse association between 25(OH)D levels and breast cancer risk was observed among women who were
PMCID:3672761
PMID: 23442740
ISSN: 1465-5411
CID: 316582
Cancer causes & control. ccc. 2013:24(1):13-25.DOI: 10.1007/s10552-012-0078-8

Diabetes and risk of pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium

Elena, Joanne W; Steplowski, Emily; Yu, Kai; Hartge, Patricia; Tobias, Geoffrey S; Brotzman, Michelle J; Chanock, Stephen J; Stolzenberg-Solomon, Rachael Z; Arslan, Alan A; Bueno-de-Mesquita, H Bas; Helzlsouer, Kathy; Jacobs, Eric J; LaCroix, Andrea; Petersen, Gloria; Zheng, Wei; Albanes, Demetrius; Allen, Naomi E; Amundadottir, Laufey; Bao, Ying; Boeing, Heiner; Boutron-Ruault, Marie-Christine; Buring, Julie E; Gaziano, J Michael; Giovannucci, Edward L; Duell, Eric J; Hallmans, Goran; Howard, Barbara V; Hunter, David J; Hutchinson, Amy; Jacobs, Kevin B; Kooperberg, Charles; Kraft, Peter; Mendelsohn, Julie B; Michaud, Dominique S; Palli, Domenico; Phillips, Lawrence S; Overvad, Kim; Patel, Alpa V; Sansbury, Leah; Shu, Xiao-Ou; Simon, Michael S; Slimani, Nadia; Trichopoulos, Dimitrios; Visvanathan, Kala; Virtamo, Jarmo; Wolpin, Brian M; Zeleniuch-Jacquotte, Anne; Fuchs, Charles S; Hoover, Robert N; Gross, Myron
PURPOSE: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). METHODS: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. RESULTS: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). CONCLUSIONS: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.
PMCID:3529822
PMID: 23112111
ISSN: 0957-5243
CID: 216052
PLoS one. 2013:8(7).DOI: 10.1371/journal.pone.0069367

Genetic variants in hormone-related genes and risk of breast cancer

Clendenen, Tess; Zeleniuch-Jacquotte, Anne; Wirgin, Isaac; Koenig, Karen L; Afanasyeva, Yelena; Lundin, Eva; Arslan, Alan A; Axelsson, Tomas; Forsti, Asta; Hallmans, Goran; Hemminki, Kari; Lenner, Per; Roy, Nirmal; Shore, Roy E; Chen, Yu
Sex hormones play a key role in the development of breast cancer. Certain polymorphic variants (SNPs and repeat polymorphisms) in hormone-related genes are associated with sex hormone levels. However, the relationship observed between these genetic variants and breast cancer risk has been inconsistent. We conducted a case-control study nested within two prospective cohorts to assess the relationship between specific genetic variants in hormone-related genes and breast cancer risk. In total, 1164 cases and 2111 individually-matched controls were included in the study. We did not observe an association between potential functional genetic polymorphisms in the estrogen pathway, SHBG rs6259, ESR1 rs2234693, CYP19 rs10046 and rs4775936, and UGT1A1 rs8175347, or the progesterone pathway, PGR rs1042838, with the risk of breast cancer. Our results suggest that these genetic variants do not have a strong effect on breast cancer risk.
PMCID:3720532
PMID: 23935996
ISSN: 1932-6203
CID: 495042