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1. Analgesic Use and Ovarian Cancer Risk: An Analysis in the Ovarian Cancer Cohort Consortium

Author

Trabert, B, Poole, EM, White, E, Visvanathan, K, Adami, HO, Anderson, GL, Brasky, TM, Brinton, LA, Fortner, RT, Gaudet, M, Hartge, P, Hoffman-Bolton, J, Jones, M, Lacey, JV, Larsson, SC, Mackenzie, GG, Schouten, LJ, Sandler, DP, O'Brien, K, Patel, AV, Peters, U, Prizment, A, Robien, K, Setiawan, WV, Swerdlow, A, Van Den Brandt, PA, Weiderpass, E, Wilkens, LR, Wolk, A, Wentzensen, N, and Tworoger, SS

Subjects
Cancer, Paediatrics and Reproductive Medicine, Obstetrics & Reproductive Medicine
Published
2018

2. Epithelial-Mesenchymal Transition (EMT) Gene Variants and Epithelial Ovarian Cancer (EOC) Risk

Author

Amankwah, EK, Lin, HY, Tyrer, JP, Lawrenson, K, Dennis, J, Chornokur, G, Aben, KKH, Anton-Culver, H, Antonenkova, N, Bruinsma, F, Bandera, EV, Bean, YT, Beckmann, MW, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bunker, CH, Butzow, R, Campbell, IG, Carty, K, Chen, Z, Chen, YA, Chang-Claude, J, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, du Bois, A, Despierre, E, Dicks, E, Doherty, JA, Dörk, T, Dürst, M, Easton, DF, Eccles, DM, Edwards, RP, Ekici, AB, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goodman, MT, Gronwald, J, Harrington, P, Harter, P, Hasmad, HN, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, CK, Hogdall, E, Hosono, S, Iversen, ES, Jakubowska, A, Jensen, A, Ji, BT, Karlan, BY, Jim, H, Kellar, M, Kiemeney, LA, Krakstad, C, Kjaer, SK, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, Le, ND, Lee, AW, Lele, S, Leminen, A, Lester, J, Levine, DA, Liang, D, Lim, BK, Lissowska, J, Lu, K, Lubinski, J, Lundvall, L, Massuger, LFAG, Matsuo, K, Mcguire, V, Mclaughlin, JR, Mcneish, I, Menon, U, Milne, RL, Modugno, F, Moysich, KB, Ness, RB, Nevanlinna, H, Eilber, U, Odunsi, K, Olson, SH, Orlow, I, Orsulic, S, and Weber, RP

Subjects
Epidemiology, Public Health and Health Services, Genetics
Abstract

Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells assume mesenchymal characteristics to facilitate cancer metastasis. However, EMT also contributes to the initiation and development of primary tumors. Prior studies that explored the hypothesis that EMT gene variants contribute to epithelial ovarian carcinoma (EOC) risk have been based on small sample sizes and none have sought replication in an independent population. We screened 15,816 single-nucleotide polymorphisms (SNPs) in 296 genes in a discovery phase using data from a genome-wide association study of EOC among women of European ancestry (1,947 cases and 2,009 controls) and identified 793 variants in 278 EMT-related genes that were nominally (P < 0.05) associated with invasive EOC. These SNPs were then genotyped in a larger study of 14,525 invasive-cancer patients and 23,447 controls. A P-value

Published
2015

3. Obesity and survival among women with ovarian cancer: results from the Ovarian Cancer Association Consortium

Author

Nagle, CM, Dixon, SC, Jensen, A, Kjaer, SK, Modugno, F, deFazio, A, Fereday, S, Hung, J, Johnatty, SE, Fasching, PA, Beckmann, MW, Lambrechts, D, Vergote, I, Van Nieuwenhuysen, E, Lambrechts, S, Risch, HA, Rossing, MA, Doherty, JA, Wicklund, KG, Chang-Claude, J, Goodman, MT, Ness, RB, Moysich, K, Heitz, F, du Bois, A, Harter, P, Schwaab, I, Matsuo, K, Hosono, S, Goode, EL, Vierkant, RA, Larson, MC, Fridley, BL, Høgdall, C, Schildkraut, JM, Weber, RP, Cramer, DW, Terry, KL, Bandera, EV, Paddock, L, Rodriguez-Rodriguez, L, Wentzensen, N, Yang, HP, Brinton, LA, Lissowska, J, Høgdall, E, Lundvall, L, Whittemore, A, McGuire, V, Sieh, W, Rothstein, J, Sutphen, R, Anton-Culver, H, Ziogas, A, Pearce, CL, Wu, AH, and Webb, PM

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Nutrition, Ovarian Cancer, Obesity, Rare Diseases, Cancer, Body Mass Index, Carcinoma, Ovarian Epithelial, Disease-Free Survival, Female, Humans, Kaplan-Meier Estimate, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, ovarian cancer, obesity, overall survival, progression-free survival, ovarian cancer-specific survival, Australian Ovarian Cancer Study Group, Ovarian Cancer Association Consortium, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundObservational studies have reported a modest association between obesity and risk of ovarian cancer; however, whether it is also associated with survival and whether this association varies for the different histologic subtypes are not clear. We undertook an international collaborative analysis to assess the association between body mass index (BMI), assessed shortly before diagnosis, progression-free survival (PFS), ovarian cancer-specific survival and overall survival (OS) among women with invasive ovarian cancer.MethodsWe used original data from 21 studies, which included 12 390 women with ovarian carcinoma. We combined study-specific adjusted hazard ratios (HRs) using random-effects models to estimate pooled HRs (pHR). We further explored associations by histologic subtype.ResultsOverall, 6715 (54%) deaths occurred during follow-up. A significant OS disadvantage was observed for women who were obese (BMI: 30-34.9, pHR: 1.10 (95% confidence intervals (CIs): 0.99-1.23); BMI: ⩾35, pHR: 1.12 (95% CI: 1.01-1.25)). Results were similar for PFS and ovarian cancer-specific survival. In analyses stratified by histologic subtype, associations were strongest for women with low-grade serous (pHR: 1.12 per 5 kg m(-2)) and endometrioid subtypes (pHR: 1.08 per 5 kg m(-2)), and more modest for the high-grade serous (pHR: 1.04 per 5 kg m(-2)) subtype, but only the association with high-grade serous cancers was significant.ConclusionsHigher BMI is associated with adverse survival among the majority of women with ovarian cancer.

Published
2015

4. Anti-Müllerian hormone and risk of ovarian cancer in nine cohorts

Author

Jung, S, Allen, N, Arslan, AA, Baglietto, L, Barricarte, A, Brinton, LA, Egleston, BL, Falk, RT, Fortner, RT, Helzlsouer, KJ, Gao, Y, Idahl, A, Kaaks, R, Krogh, V, Merritt, MA, Lundin, E, Onland-Moret, NC, Rinaldi, S, Schock, H, Shu, X-O, Sluss, PM, Staats, PN, Sacerdote, C, Travis, RC, Tjønneland, A, Trichopoulou, A, Tworoger, SS, Visvanathan, K, Weiderpass, E, Zeleniuch-Jacquotte, A, and Dorgan, JF

Subjects
Adult, Anti-Mullerian Hormone, Cancer Research, endocrine system, endocrine system diseases, Cystadenocarcinoma, ovarian function, Adenocarcinoma, Article, Clear Cell, Cohort Studies, Young Adult, Journal Article, Humans, Mucinous, Neoplasm Staging, Ovarian Neoplasms, Serous, Middle Aged, anti-Müllerian hormone, epidemiology, ovarian cancer, Adenocarcinoma, Clear Cell, Adenocarcinoma, Mucinous, Biomarkers, Case-Control Studies, Cystadenocarcinoma, Serous, Endometrial Neoplasms, Female, Follow-Up Studies, Neoplasm Grading, Premenopause, Prognosis, Oncology, female genital diseases and pregnancy complications
Abstract

Animal and experimental data suggest that anti-Müllerian hormone (AMH) serves as a marker of ovarian reserve and inhibits the growth of ovarian tumors. However, few epidemiologic studies have examined the association between AMH and ovarian cancer risk. We conducted a nested case-control study of 302 ovarian cancer cases and 336 matched controls from nine cohorts. Prediagnostic blood samples of premenopausal women were assayed for AMH using a picoAMH enzyme-linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted conditional logistic regression. AMH concentration was not associated with overall ovarian cancer risk. The multivariable-adjusted OR (95% CI), comparing the highest to the lowest quartile of AMH, was 0.99 (0.59-1.67) (Ptrend : 0.91). The association did not differ by age at blood draw or oral contraceptive use (all Pheterogeneity : ≥0.26). There also was no evidence for heterogeneity of risk for tumors defined by histologic developmental pathway, stage, and grade, and by age at diagnosis and time between blood draw and diagnosis (all Pheterogeneity : ≥0.39). In conclusion, this analysis of mostly late premenopausal women from nine cohorts does not support the hypothesized inverse association between prediagnostic circulating levels of AMH and risk of ovarian cancer.

Published
2019

5. Variants in genes encoding small GTPases and association with epithelial ovarian cancer susceptibility

Author

Earp, M, Tyrer, JP, Winham, SJ, Lin, HY, Chornokur, G, Dennis, J, Aben, KKH, Anton-Culver, H, Antonenkova, N, Bandera, EV, Bean, YT, Beckmann, MW, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bruinsma, F, Bunker, CH, Butzow, R, Campbell, IG, Carty, K, Chang-Claude, J, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, Despierre, E, Doherty, JA, Dörk, T, Du Bois, A, Dürst, M, Easton, DF, Eccles, DM, Edwards, RP, Ekici, AB, Fasching, PA, Fridley, BL, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goodman, MT, Gronwald, J, Harter, P, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, CK, Høgdall, E, Hosono, S, Iversen, ES, Jakubowska, A, Jensen, A, Ji, BT, Jung, AY, Karlan, BY, Kellar, M, Kiemeney, LA, Lim, BK, Kjaer, SK, Krakstad, C, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, Le, ND, Lele, S, Lester, J, Levine, DA, Li, Z, Liang, D, Lissowska, J, Lu, K, Lubinski, J, Lundvall, L, Massuger, LFAG, Matsuo, K, and McGuire, V

Subjects
endocrine system diseases, female genital diseases and pregnancy complications
Abstract

© This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Epithelial ovarian cancer (EOC) is the fifth leading cause of cancer mortality in American women. Normal ovarian physiology is intricately connected to small GTP binding proteins of the Ras superfamily (Ras, Rho, Rab, Arf, and Ran) which govern processes such as signal transduction, cell proliferation, cell motility, and vesicle transport. We hypothesized that common germline variation in genes encoding small GTPases is associated with EOC risk. We investigated 322 variants in 88 small GTPase genes in germline DNA of 18,736 EOC patients and 26,138 controls of European ancestry using a custom genotype array and logistic regression fitting log-additive models. Functional annotation was used to identify bio-features and expression quantitative trait loci that intersect with risk variants. One variant, ARHGEF10L (Rho guanine nucleotide exchange factor 10 like) rs2256787, was associated with increased endometrioid EOC risk (OR = 1.33, p = 4.46 x 10−6). Other variants of interest included another in ARHGEF10L, rs10788679, which was associated with invasive serous EOC risk (OR = 1.07, p = 0.00026) and two variants in AKAP6 (A-kinase anchoring protein 6) which were associated with risk of invasive EOC (rs1955513, OR = 0.90, p = 0.00033; rs927062, OR = 0.94, p = 0.00059). Functional annotation revealed that the two ARHGEF10L variants were located in super-enhancer regions and that AKAP6 rs927062 was associated with expression of GTPase gene ARHGAP5 (Rho GTPase activating protein 5). Inherited variants in ARHGEF10L and AKAP6, with potential transcriptional regulatory function and association with EOC risk, warrant investigation in independent EOC study populations.

Published
2018

6. Circulating Anti-Müllerian Hormone and Breast Cancer Risk: A Study in Ten Prospective Cohorts

Author

Ge, W, Clendenen, TV, Afanasyeva, Y, Koenig, KL, Agnoli, C, Brinton, LA, Dorgan, JF, Eliassen, AH, Falk, RT, Hallmans, G, Hankinson, SE, Hoffman-Bolton, J, Key, TJ, Krogh, V, Nichols, HB, Sandler, DP, Schoemaker, MJ, Sluss, PM, Sund, M, Swerdlow, AJ, Visvanathan, K, Liu, M, and Zeleniuch-Jacquotte, A

Subjects
Adult, Anti-Mullerian Hormone, Breast Neoplasms, Middle Aged, Risk Assessment, Article, Logistic Models, Risk Factors, Case-Control Studies, Odds Ratio, Humans, Female, Prospective Studies, Aged
Abstract

A strong positive association has been observed between circulating anti-Müllerian hormone (AMH), a biomarker of ovarian reserve, and breast cancer risk in three prospective studies. Confirming this association is important because of the paucity of biomarkers of breast cancer risk in premenopausal women. We conducted a consortium study including ten prospective cohorts that had collected blood from premenopausal women. A nested case-control design was implemented within each cohort. A total of 2,835 invasive (80%) and in situ (20%) breast cancer cases were individually matched to controls (n = 3,122) on age at blood donation. AMH was measured using a high sensitivity enzyme-linked immunoabsorbent assay. Conditional logistic regression was applied to the aggregated dataset. There was a statistically significant trend of increasing breast cancer risk with increasing AMH concentration (p(trend) across quartiles < 0.0001) after adjusting for breast cancer risk factors. The odds ratio (OR) for breast cancer in the top versus bottom quartile of AMH was 1.60 (95% CI = 1.31-1.94). Though the test for interaction was not statistically significant (p(interaction) = 0.15), the trend was statistically significant only for tumors positive for both estrogen receptor (ER) and progesterone receptor (PR): ER+/PR+: OR(Q4-Q1) = 1.96, 95% CI = 1.46-2.64, p(trend)

Published
2018

7. Abstract P1-08-04: Withdrawn

Author

Trabert, B, primary, Bauer, DC, additional, Brinton, LA, additional, Buist, DS, additional, Cauley, JA, additional, Dallal, CM, additional, Gierach, GL, additional, Falk, RT, additional, Hue, TF, additional, Lacey, JV, additional, LaCroix, AZ, additional, Tice, JA, additional, and Xu, X, additional

Published
2019
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8. Ovarian cancer and smoking: individual participant meta-analysis including 28,114 women with ovarian cancer from 51 epidemiological studies

Author

Gaitskell, K, Hermon, C, Moser, K, Reeves, G, Peto, R, Brinton, L, Marchbanks, P, Negri, E, Ness, R, Peeters, PHM, Vessey, M, Calle, EE, Gapstur, SM, Patel, AV, Dal Maso, L, Talamini, R, Chetrit, A, Hirsh-Yechezkel, G, Lubin, F, Sadetzki, S, Banks, E, Beral, V, Bull, D, Callaghan, K, Crossley, B, Goodill, A, Green, J, Key, T, Sitas, F, Collins, R, Doll, R, Gonzalez, A, Lee, N, Ory, HW, Peterson, HB, Wingo, PA, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Tjonneland, A, Titus-Ernstoff, L, Byers, T, Rohan, T, Mosgaard, BJ, Yeates, D, Freudenheim, JL, Chang-Claude, J, Kaaks, R, Anderson, KE, Folsom, A, Robien, K, Hampton, J, Newcomb, PA, Rossing, MA, Thomas, DB, Weiss, NS, Riboli, E, Clavel-Chapelon, F, Cramer, D, Hankinson, SE, Tworoger, SS, Franceschi, S, La Vecchia, C, Adami, HO, Magnusson, C, Riman, T, Weiderpass, Elisabete, Wolk, A, Schouten, LJ, van den Brandt, PA, Chantarakul, N, Koetsawang, S, Rachawat, D, Palli, D, Black, A, Brinton, LA, Freedman, DM, Hartge, P, Hsing, AW, Lacey, JV, Hoover, RN, Schairer, C, Urban, M, Graff-Iversen, Sidsel, Selmer, Randi, Bain, CJ, Green, AC, Purdie, DM, Siskind, V, Webb, PM, Moysich, K, McCann, SE, Hannaford, P, Kay, C, Binns, CW, Lee, AH, Zhang, M, Ness, RB, Nasca, P, Coogan, PF, Palmer, JR, Rosenberg, L, Kelsey, J, Paffenbarger, R, Whittemore, A, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Tzonou, A, Dabancens, A, Martinez, L, Molina, R, Salas, O, Goodman, MT, Lurie, G, Carney, ME, Wilkens, LR, Hartman, L, Manjer, J, Olsson, H, Grisso, JA, Morgan, M, Wheeler, JE, Bunker, CH, Edwards, RP, Modugno, F, Casagrande, J, Pike, MC, Ross, RK, Wu, AH, Miller, AB, Kumle, Merethe, Gram, Inger Torhild, Lund, Eiliv, McGowan, L, Shu, XO, Zheng, W, Farley, TMM, Holck, S, Meirik, O, Risch, HA, E. E. Calle, S. M. Gapstur, A. V. Patel, L. Dal Maso, R. Talamini, A. Chetrit, G. Hirsh Yechezkel, F. Lubin, S. Sadetzki, E. Bank, V. Beral, D. Bull, K. Callaghan, B. Crossley, K. Gaitskell, A. Goodill, J. Green, C. Hermon, T. Key, K. Moser, G. Reeve, F. Sita, R. Collin, R. Doll, R. Peto, C. A. Gonzalez, N. Lee, P. Marchbank, H. W. Ory, H. B. Peterson, P. A. Wingo, N. Martin, T. Pardthaisong, S. Silpisornkosol, C. Theetranont, B. Boosiri, S. Chutivongse, P. Jimakorn, P. Virutamasen, C. Wongsrichanalai, A. Tjonneland, L. Titus Ernstoff, T. Byer, T. Rohan, B. J. Mosgaard, M. Vessey, D. Yeate, J. L. Freudenheim, J. Chang Claude, R. Kaak, K. E. Anderson, A. Folsom, K. Robien, J. Hampton, P. A. Newcomb, M. A. Rossing, D. B. Thoma, N. S. Wei, E. Riboli, F. Clavel Chapelon, D. Cramer, S. E. Hankinson, S. S. Tworoger, S. Franceschi, C. La Vecchia, E. Negri, H. O. Adami, C. Magnusson, T. Riman, E. Weiderpa, A. Wolk, L. J. Schouten, P. A. van den Brandt, N. Chantarakul, S. Koetsawang, D. Rachawat, D. Palli, A. Black, L. A. Brinton, D. M. Freedman, P. Hartge, A. W. Hsing, J. Lacey, R. N. Hoover, C. Schairer, M. Urban, S. Graff Iversen, R. Selmer, C. J. Bain, A. C. Green, D. M. Purdie, V. Siskind, P. M. Webb, K. Moysich, S. E. Mccann, P. Hannaford, C. Kay, C. W. Binn, A. H. Lee, M. Zhang, R. B. Ne, P. Nasca, P. F. Coogan, J. R. Palmer, L. Rosenberg, J. Kelsey, R. Paffenbarger, A. Whittemore, K. Katsouyanni, A. Trichopoulou, D. Trichopoulo, A. Tzonou, A. Dabancen, L. Martinez, R. Molina, O. Sala, M. T. Goodman, G. Lurie, M. E. Carney, L. R. Wilken, L. Hartman, J. Manjer, H. Olsson, J. A. Grisso, M. Morgan, J. E. Wheeler, C. H. Bunker, R. P. Edward, F. Modugno, P. H. M. Peeter, J. Casagrande, M. C. Pike, R. K. Ro, A. H. Wu, A. B. Miller, M. Kumle, I. T. Gram, E. Lund, L. Mcgowan, X. O. Shu, W. Zheng, T. M. M. Farley, S. Holck, O. Meirik, H. A. Risch, Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, and RS: GROW - School for Oncology and Reproduction

Subjects
hormonal factor, Oncology, body-mass index, Comorbidity, anthropometric measurement, Body Mass Index, 0302 clinical medicine, Epidemiology, Cancer Type - Ovarian Cancer, 030212 general & internal medicine, epithelial ovarian, Prospective cohort study, oral contraceptives, Ovarian Neoplasms, Incidence (epidemiology), Incidence, Smoking, Articles, Middle Aged, Adenocarcinoma, Mucinous, 3. Good health, Causality, Europe, risk-factor, Serous fluid, 030220 oncology & carcinogenesis, Meta-analysis, Adenocarcinoma, Female, Risk, Adult, medicine.medical_specialty, prospective cohort, Etiology - Exogenous Factors in the Origin and Cause of Cancer, Risk Assessment, methods, 03 medical and health sciences, Internal medicine, oral-contraceptive use, medicine, cancer, Humans, Women, tobacco smoking, therapy, cigarette-smoking, VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762, business.industry, Research, medicine.disease, VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762, Relative risk, North America, Other, United-State, business, Ovarian cancer, Meta-Analysis
Abstract

BACKGROUND: Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. METHODS: Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28,114 women with and 94,942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. FINDINGS: After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1·06, 95% CI 1·01-1·11, p=0·01). Of 17,641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p(heterogeneity)

Published
2016

9. Inherited variants affecting RNA editing may contribute to ovarian cancer susceptibility: Results from a large-scale collaboration

Author

Permuth, JB, Reid, B, Earp, M, Chen, YA, Monteiro, ANA, Chen, Z, Chenevix-Trench, G, Fasching, PA, Beckmann, MW, Lambrechts, D, Vanderstichele, A, Van Niewenhuyse, E, Vergote, I, Rossing, MA, Doherty, JA, Chang-Claude, J, Moysich, K, Odunsi, K, Goodman, MT, Shvetsov, YB, Wilkens, LR, Thompson, PJ, Dörk, T, Bogdanova, N, Butzow, R, Nevanlinna, H, Pelttari, L, Leminen, A, Modugno, F, Edwards, RP, Ness, RB, Kelley, J, Heitz, F, Karlan, B, Lester, J, Kjaer, SK, Jensen, A, Giles, G, Hildebrandt, M, Liang, D, Lu, KH, Wu, X, Levine, DA, Bisogna, M, Berchuck, A, Cramer, DW, Terry, KL, Tworoger, SS, Poole, EM, Bandera, EV, Fridley, B, Cunningham, J, Winham, SJ, Olson, SH, Orlow, I, Bjorge, L, Kiemeney, LA, Massuger, L, Pejovic, T, Moffitt, M, Le, N, Cook, LS, Brooks-Wilson, A, Kelemen, LE, Gronwald, J, Lubinski, J, Wentzensen, N, Brinton, LA, Lissowska, J, Yang, H, Hogdall, E, Hogdall, C, Lundvall, L, Pharoah, PDP, Song, H, Campbell, I, Eccles, D, and McNeish, I

Abstract

RNA editing in mammals is a form of post-transcriptional modification in which adenosine is converted to inosine by the adenosine deaminases acting on RNA (ADAR) family of enzymes. Based on evidence of altered ADAR expression in epithelial ovarian cancers (EOC), we hypothesized that single nucleotide polymorphisms (SNPs) in ADAR genes modify EOC susceptibility, potentially by altering ovarian tissue gene expression. Using directly genotyped and imputed data from 10,891 invasive EOC cases and 21,693 controls, we evaluated the associations of 5,303 SNPs in ADAD1, ADAR, ADAR2, ADAR3, and SND1. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI), with adjustment for European ancestry. We conducted gene-level analyses using the Admixture Maximum Likelihood (AML) test and the Sequence-Kernel Association test for common and rare variants (SKAT-CR). Association analysis revealed top risk-associated SNP rs77027562 (OR (95% CI)= 1.39 (1.17-1.64), P=1.0x10-4) in ADAR3 and rs185455523 in SND1 (OR (95% CI)= 0.68 (0.56-0.83), P=2.0x10-4). When restricting to serous histology (n=6,500), the magnitude of association strengthened for rs185455523 (OR=0.60, P=1.0x10-4). Gene-level analyses revealed that variation in ADAR was associated (P

Published
2016

10. Assessment of variation in immunosuppressive pathway genes reveals TGFBR2 to be associated with risk of clear cell ovarian cancer

Author

Hampras, SS, Sucheston-Campbell, LE, Cannioto, R, Chang-Claude, J, Modugno, F, Dörk, T, Hillemanns, P, Preus, L, Knutson, KL, Wallace, PK, Hong, CC, Friel, G, Davis, W, Nesline, M, Pearce, CL, Kelemen, LE, Goodman, MT, Bandera, EV, Terry, KL, Schoof, N, Eng, KH, Clay, A, Singh, PK, Joseph, JM, Aben, KKH, Anton-Culver, H, Antonenkova, N, Baker, H, Bean, Y, Beckmann, MW, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bruinsma, F, Butzow, R, Campbell, IG, Carty, K, Cook, LS, Cramer, DW, Cybulski, C, Dansonka-Mieszkowska, A, Dennis, J, Despierre, E, Dicks, E, Doherty, JA, du Bois, A, Dürst, M, Easton, D, Eccles, D, Edwards, RP, Ekici, AB, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Gronwald, J, Harrington, P, Harter, P, Hasmad, HN, Hein, A, Heitz, F, Hildebrandt, MAT, Hogdall, C, Hogdall, E, Hosono, S, Iversen, ES, Jakubowska, A, Jensen, A, Ji, BT, Karlan, BY, Kellar, M, Kelley, JL, Kiemeney, LA, Klapdor, R, Kolomeyevskaya, N, Krakstad, C, Kjaer, SK, Kruszka, B, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, Le, ND, Lee, AW, Lele, S, Leminen, A, Lester, J, Levine, DA, Liang, D, Lissowska, J, Liu, S, and Lu, K

Subjects
endocrine system diseases, female genital diseases and pregnancy complications
Abstract

Background: Regulatory T (Treg) cells, a subset of CD4+ T lymphocytes, are mediators of immunosuppression in cancer, and, thus, variants in genes encoding Treg cell immune molecules could be associated with ovarian cancer. Methods: In a population of 15,596 epithelial ovarian cancer (EOC) cases and 23,236 controls, we measured genetic associations of 1,351 SNPs in Treg cell pathway genes with odds of ovarian cancer and tested pathway and gene-level associations, overall and by histotype, for the 25 genes, using the admixture likelihood (AML) method. The most significant single SNP associations were tested for correlation with expression levels in 44 ovarian cancer patients. Results: The most significant global associations for all genes in the pathway were seen in endometrioid (p = 0.082) and clear cell (p = 0.083), with the most significant gene level association seen with TGFBR2 (p = 0.001) and clear cell EOC. Gene associations with histotypes at p < 0.05 included: IL12 (p = 0.005 and p = 0.008, serous and high-grade serous, respectively), IL8RA (p = 0.035, endometrioid and mucinous), LGALS1 (p = 0.03, mucinous), STAT5B (p = 0.022, clear cell), TGFBR1 (p = 0.021 endometrioid) and TGFBR2 (p = 0.017 and p = 0.025, endometrioid and mucinous, respectively). Conclusions: Common inherited gene variation in Treg cell pathways shows some evidence of germline genetic contribution to odds of EOC that varies by histologic subtype and may be associated with mRNA expression of immune-complex receptor in EOC patients.

Published
2016

11. Cis-eQTL analysis and functional validation of candidate susceptibility genes for high-grade serous ovarian cancer

Author

Lawrenson, K, Li, Q, Kar, S, Seo, JH, Tyrer, J, Spindler, TJ, Lee, J, Chen, Y, Karst, A, Drapkin, R, Aben, KKH, Anton-Culver, H, Antonenkova, N, Baker, H, Bandera, EV, Bean, Y, Beckmann, MW, Berchuck, A, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bruinsma, F, Butzow, R, Campbell, IG, Carty, K, Chang-Claude, J, Chenevix-Trench, G, Chen, A, Chen, Z, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, Dennis, J, Dicks, E, Doherty, JA, Dörk, T, Du Bois, A, Dürst, M, Eccles, D, Easton, DT, Edwards, RP, Eilber, U, Ekici, AB, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goode, EL, Goodman, MT, Grownwald, J, Harrington, P, Harter, P, Hasmad, HN, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, E, Hogdall, C, Hosono, S, Iversen, ES, Jakubowska, A, James, P, Jensen, A, Ji, BT, Karlan, BY, Kjaer, SK, Kelemen, LE, Kellar, M, Kelley, JL, Kiemeney, LA, Krakstad, C, Kupryjanczyk, J, and Lambrechts, D

Abstract

© 2015 Macmillan Publishers Limited. All rights reserved. Genome-wide association studies have reported 11 regions conferring risk of high-grade serous epithelial ovarian cancer (HGSOC). Expression quantitative trait locus (eQTL) analyses can identify candidate susceptibility genes at risk loci. Here we evaluate cis-eQTL associations at 47 regions associated with HGSOC risk (P≤10-5). For three cis-eQTL associations (P

Published
2015

12. Cell-type-specific enrichment of risk-associated regulatory elements at ovarian cancer susceptibility loci

Author

Coetzee, SG, Shen, HC, Hazelett, DJ, Lawrenson, K, Kuchenbaecker, K, Tyrer, J, Rhie, SK, Levanon, K, Karst, A, Drapkin, R, Ramus, SJ, Couch, FJ, Offit, K, Chenevix-Trench, G, Monteiro, ANA, Antoniou, A, Freedman, M, Coetzee, GA, Pharoah, PDP, Noushmehr, H, Gayther, SA, Anton-Culver, H, Antonenkova, N, Baker, H, Bandera, EV, Bean, Y, Beckmann, MW, Berchuck, A, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bruinsma, F, Butzow, R, Campbell, IG, Carty, K, Chang-Claude, J, Chen, A, Chen, Z, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, Dennis, J, Dicks, E, Doherty, JA, Dörk, T, Bois, AD, Dürst, M, Eccles, D, Easton, DF, Edwards, RP, Eilber, U, Ekici, AB, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goode, EL, Goodman, MT, Grownwald, J, Harrington, P, Harter, P, Hasmad, HN, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, E, Hogdall, C, Hosono, S, Iversen, ES, Jakubowska, A, James, P, Jensen, A, Ji, BT, Karlan, BY, Kjaer, SK, Kelemen, LE, Kellar, M, Kelley, JL, Kiemeney, LA, Krakstad, C, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, Le, ND, Lele, S, Leminen, A, and Lester, J

Abstract

© The Author 2015. Published by Oxford University Press. All rights reserved. Understanding the regulatory landscape of the human genome is a central question in complex trait genetics. Most singlenucleotide polymorphisms (SNPs) associated with cancer risk lie in non-protein-coding regions, implicating regulatory DNA elements as functional targets of susceptibility variants. Here, we describe genome-wide annotation of regions of open chromatin and histone modification in fallopian tube and ovarian surface epithelial cells (FTSECs, OSECs), the debated cellular origins of high-grade serous ovarian cancers (HGSOCs) and in endometriosis epithelial cells (EECs), the likely precursor of clear cell ovarian carcinomas (CCOCs). The regulatory architecture of these cell types was compared with normal human mammary epithelial cells and LNCaP prostate cancer cells. We observed similar positional patterns of global enhancer signatures across the three different ovarian cancer precursor cell types, and evidence of tissue-specific regulatory signatures compared to nongynecological cell types. We found significant enrichment for risk-associated SNPs intersecting regulatory biofeatures at 17 known HGSOC susceptibility loci in FTSECs (P = 3.8 × 10-30), OSECs (P = 2.4 × 10-23) and HMECs (P = 6.7 × 10-15) but not for EECs (P = 0.45) or LNCaP cells (P = 0.88). Hierarchical clustering of risk SNPs conditioned on the six different cell types indicates FTSECs and OSECs are highly related (96% of samples using multi-scale bootstrapping) suggesting both cell types may be precursors of HGSOC. These data represent the first description of regulatory catalogues of normal precursor cells for different ovarian cancer subtypes, and provide unique insights into the tissue specific regulatory variation with respect to the likely functional targets of germline genetic susceptibility variants for ovarian cancer.

Published
2015

13. Common genetic variation in cellular transport genes and epithelial ovarian cancer (EOC) risk

Author

Chornokur, G, Lin, HY, Tyrer, JP, Lawrenson, K, Dennis, J, Amankwah, EK, Qu, X, Tsai, YY, Jim, HSL, Chen, Z, Chen, AY, Permuth-Wey, J, Aben, KKH, Anton-Culver, H, Antonenkova, N, Bruinsma, F, Bandera, EV, Bean, YT, Beckmann, MW, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bunker, CH, Butzow, R, Campbell, IG, Carty, K, Chang-Claude, J, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, Du Bois, A, Despierre, E, Dicks, E, Doherty, JA, Dörk, T, Dürst, M, Easton, DF, Eccles, DM, Edwards, RP, Ekici, AB, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goodman, MT, Gronwald, J, Harrington, P, Harter, P, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, CK, Hogdall, E, Hosono, S, Jakubowska, A, Jensen, A, Ji, BT, Karlan, BY, Kelemen, LE, Kellar, M, Kiemeney, LA, Krakstad, C, Kjaer, SK, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, Le, ND, Lee, AW, Lele, S, Leminen, A, and Lester, J

Abstract

© 2015 Chornokur et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Background: Defective cellular transport processes can lead to aberrant accumulation of trace elements, iron, small molecules and hormones in the cell, which in turn may promote the formation of reactive oxygen species, promoting DNA damage and aberrant expression of key regulatory cancer genes. As DNA damage and uncontrolled proliferation are hallmarks of cancer, including epithelial ovarian cancer (EOC), we hypothesized that inherited variation in the cellular transport genes contributes to EOC risk. Methods: In total, DNA samples were obtained from 14,525 case subjects with invasive EOC and from 23,447 controls from 43 sites in the Ovarian Cancer Association Consortium (OCAC). Two hundred seventy nine SNPs, representing 131 genes, were genotyped using an Illumina Infinium iSelect BeadChip as part of the Collaborative Oncological Gene-environment Study (COGS). SNP analyses were conducted using unconditional logistic regression under a log-additive model, and the FDR q-4). Conclusion: These results, generated on a large cohort of women, revealed associations between inherited cellular transport gene variants and risk of EOC histologic subtypes.

Published
2015

14. Genome-wide significant risk associations for mucinous ovarian carcinoma

Author

Kelemen, LE, Lawrenson, K, Tyrer, J, Li, Q, Lee, JM, Seo, JH, Phelan, CM, Beesley, J, Chen, X, Spindler, TJ, Aben, KKH, Anton-Culver, H, Antonenkova, N, Baker, H, Bandera, EV, Bean, Y, Beckmann, MW, Bisogna, M, Bjorge, L, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Bruinsma, F, Butzow, R, Campbell, IG, Carty, K, Chang-Claude, J, Chen, YA, Chen, Z, Cook, LS, Cramer, DW, Cunningham, JM, Cybulski, C, Dansonka-Mieszkowska, A, Dennis, J, Dicks, E, Doherty, JA, Dörk, T, Bois, AD, Dürst, M, Eccles, D, Easton, DT, Edwards, RP, Eilber, U, Ekici, AB, Engelholm, SA, Fasching, PA, Fridley, BL, Gao, YT, Gentry-Maharaj, A, Giles, GG, Glasspool, R, Goode, EL, Goodman, MT, Grownwald, J, Harrington, P, Harter, P, Hasmad, HN, Hein, A, Heitz, F, Hildebrandt, MAT, Hillemanns, P, Hogdall, E, Hogdall, C, Hosono, S, Iversen, ES, Jakubowska, A, Jensen, A, Ji, BT, Karlan, BY, Kellar, M, Kelley, JL, Kiemeney, LA, Krakstad, C, Kjaer, SK, Kupryjanczyk, J, Lambrechts, D, Lambrechts, S, and Le, ND

Abstract

© 2015 Nature America, Inc. All rights reserved. Genome-wide association studies have identified several risk associations for ovarian carcinomas but not for mucinous ovarian carcinomas (MOCs). Our analysis of 1,644 MOC cases and 21,693 controls with imputation identified 3 new risk associations: rs752590 at 2q13 (P = 3.3 × 10-8), rs711830 at 2q31.1 (P = 7.5 × 10-12) and rs688187 at 19q13.2 (P = 6.8 × 10-13). We identified significant expression quantitative trait locus (eQTL) associations for HOXD9 at 2q31.1 in ovarian (P = 4.95 × 10-4, false discovery rate (FDR) = 0.003) and colorectal (P = 0.01, FDR = 0.09) tumors and for PAX8 at 2q13 in colorectal tumors (P = 0.03, FDR = 0.09). Chromosome conformation capture analysis identified interactions between the HOXD9 promoter and risk-associated SNPs at 2q31.1. Overexpressing HOXD9 in MOC cells augmented the neoplastic phenotype. These findings provide the first evidence for MOC susceptibility variants and insights into the underlying biology of the disease.

Published
2015

15. Circulating sex hormones and breast cancer riskfactors in postmenopausal women: reanalysis of 13 studies

Author

Endogenous Hormones, Breast Cancer Collaborative Group, Key TJ, Appleby PN, Reeves GK, Roddam AW, Helzlsouer KJ, Alberg AJ, Rollison DE, Dorgan JF, Brinton LA, Overvad K, Kaaks R, Trichopoulou A, Clavel Chapelon F, Duell EJ, Peeters PH, Rinaldi S, Fentiman IS, Dowsett M, Manjer J, Lenner P, Hallmans G, Baglietto L, English DR, Giles GG, Hopper JL, Severi G, Morris HA, Hankinson SE, Tworoger SS, Koenig K, Zeleniuch Jacquotte A, Arslan AA, Toniolo P, Shore RE, Krogh V, Micheli A, Berrino F, Barrett Connor E, Laughlin GA, Kabuto M, Akiba S, Stevens RG, Neriishi K, Land CE, Cauley JA, Lui LY, Cummings SR, Gunter MJ, Rohan TE, Strickler H.D., PANICO, SALVATORE, Endogenous, Hormone, Breast Cancer Collaborative, Group, Key, Tj, Appleby, Pn, Reeves, Gk, Roddam, Aw, Helzlsouer, Kj, Alberg, Aj, Rollison, De, Dorgan, Jf, Brinton, La, Overvad, K, Kaaks, R, Trichopoulou, A, Clavel Chapelon, F, Panico, Salvatore, Duell, Ej, Peeters, Ph, Rinaldi, S, Fentiman, I, Dowsett, M, Manjer, J, Lenner, P, Hallmans, G, Baglietto, L, English, Dr, Giles, Gg, Hopper, Jl, Severi, G, Morris, Ha, Hankinson, Se, Tworoger, S, Koenig, K, Zeleniuch Jacquotte, A, Arslan, Aa, Toniolo, P, Shore, Re, Krogh, V, Micheli, A, Berrino, F, Barrett Connor, E, Laughlin, Ga, Kabuto, M, Akiba, S, Stevens, Rg, Neriishi, K, Land, Ce, Cauley, Ja, Lui, Ly, Cummings, Sr, Gunter, Mj, Rohan, Te, and Strickler, H. D.

Published
2011

16. Variation in NF-κB signaling pathways and survival in invasive epithelial ovarian cancer

Author

Block, MS, Charbonneau, B, Vierkant, RA, Fogarty, Z, Bamlet, WR, Pharoah, PDP, Chenevix-Trench, G, Rossing, MA, Cramer, D, Pearce, CL, Schildkraut, J, Menon, U, Kjaer, SK, Levine, DA, Gronwald, J, Culver, HA, Whittemore, AS, Karlan, BY, Lambrechts, D, Wentzensen, N, Kupryjanczyk, J, Chang-Claude, J, Bandera, EV, Hogdall, E, Heitz, F, Kaye, SB, Fasching, PA, Campbell, I, Goodman, MT, Pejovic, T, Bean, YT, Hays, LE, Lurie, G, Eccles, D, Hein, A, Beckmann, MW, Ekici, AB, Paul, J, Brown, R, Flanagan, JM, Harter, P, Du Bois, A, Schwaab, I, Hogdall, CK, Lundvall, L, Olson, SH, Orlow, I, Paddock, LE, Rudolph, A, Eilber, U, Dansonka-Mieszkowska, A, Rzepecka, IK, Ziolkowska-Seta, I, Brinton, LA, Yang, H, Garcia-Closas, M, Despierre, E, Lambrechts, S, Vergote, I, Walsh, CS, Lester, J, Sieh, W, McGuire, V, Rothstein, JH, Ziogas, A, Lubinski, J, Cybulski, C, Menkiszak, J, Jensen, A, Gayther, SA, Ramus, SJ, Gentry-Maharaj, A, Berchuck, A, Wu, AH, Pike, MC, Van Den Berg, D, Terry, KL, Vitonis, AF, Ramirez, SM, Rider, DN, Knutson, KL, and Sellers, TA

Subjects
endocrine system diseases, female genital diseases and pregnancy complications
Abstract

Survival in epithelial ovarian cancer (EOC) is influenced by the host immune response, yet the key genetic determinants of inflammation and immunity that affect prognosis are not known. The nuclear factor-kB (NF-kB) transcription factor family plays an important role in many immune and inflammatory responses, including the response to cancer. We studied common inherited variation in 210 genes in the NF-kB family in 10,084 patients with invasive EOC (5,248 high-grade serous, 1,452 endometrioid, 795 clear cell, and 661 mucinous) from the Ovarian Cancer Association Consortium. Associations between genotype and overall survival were assessed using Cox regression for all patients and by major histology, adjusting for known prognostic factors and correcting for multiple testing (threshold for statistical significance, P < 2.5 × 10-5). Results were statistically significant when assessed for patients of a single histology. Key associations were with caspase recruitment domain family, member 11 (CARD11) rs41324349 in patients with mucinous EOC [HR, 1.82; 95% confidence interval (CI), 1.41-2.35; P = 4.13 × 10-6] and tumor necrosis factor receptor superfamily, member 13B (TNFRSF13B) rs7501462 in patients with endometrioid EOC (HR, 0.68; 95% CI, 0.56-0.82; P = 2.33 × 10-5). Other associations of note included TNF receptor-associated factor 2 (TRAF2) rs17250239 in patients with high-grade serous EOC (HR, 0.84; 95% CI, 0.77-0.92; P = 6.49 ± 10-5) and phospholipase C, gamma 1 (PLCG1) rs11696662 in patients with clear cell EOC (HR, 0.43; 95% CI, 0.26-0.73; P = 4.56 × 10-4). These associations highlight the potential importance of genes associated with host inflammation and immunity in modulating clinical outcomes in distinct EOC histologies. © 2014 American Association for Cancer Research.

Published
2014

17. Identification and molecular characterization of a new ovarian cancer susceptibility locus at 17q21.31

Author

Permuth-Wey, J, Lawrenson, K, Shen, HC, Velkova, A, Tyrer, JP, Chen, Z, Lin, HY, Ann Chen, Y, Tsai, YY, Qu, X, Ramus, SJ, Karevan, R, Lee, J, Lee, N, Larson, MC, Aben, KK, Anton-Culver, H, Antonenkova, N, Antoniou, AC, Armasu, SM, Bacot, F, Baglietto, L, Bandera, EV, Barnholtz-Sloan, J, Beckmann, MW, Birrer, MJ, Bloom, G, Bogdanova, N, Brinton, LA, Brooks-Wilson, A, Brown, R, Butzow, R, Cai, Q, Campbell, I, Chang-Claude, J, Chanock, S, Chenevix-Trench, G, Cheng, JQ, Cicek, MS, Coetzee, GA, Cook, LS, Couch, FJ, Cramer, DW, Cunningham, JM, Dansonka-Mieszkowska, A, Despierre, E, Doherty, JA, Dörk, T, Du Bois, A, Dürst, M, Easton, DF, Eccles, D, Edwards, R, Ekici, AB, Fasching, PA, Fenstermacher, DA, Flanagan, JM, Garcia-Closas, M, Gentry-Maharaj, A, Giles, GG, Glasspool, RM, Gonzalez-Bosquet, J, Goodman, MT, Gore, M, Górski, B, Gronwald, J, Hall, P, Halle, MK, Harter, P, Heitz, F, Hillemanns, P, Hoatlin, M, Høgdall, CK, Høgdall, E, Hosono, S, Jakubowska, A, Jensen, A, Jim, H, Kalli, KR, Karlan, BY, Kaye, SB, Kelemen, LE, Kiemeney, LA, Kikkawa, F, and Konecny, GE

Subjects
endocrine system diseases, female genital diseases and pregnancy complications
Abstract

Epithelial ovarian cancer (EOC) has a heritable component that remains to be fully characterized. Most identified common susceptibility variants lie in non-protein-coding sequences. We hypothesized that variants in the 3′ untranslated region at putative microRNA (miRNA)-binding sites represent functional targets that influence EOC susceptibility. Here, we evaluate the association between 767 miRNA-related single-nucleotide polymorphisms (miRSNPs) and EOC risk in 18,174 EOC cases and 26,134 controls from 43 studies genotyped through the Collaborative Oncological Gene-environment Study. We identify several miRSNPs associated with invasive serous EOC risk (odds ratio=1.12, P=10-8) mapping to an inversion polymorphism at 17q21.31. Additional genotyping of non-miRSNPs at 17q21.31 reveals stronger signals outside the inversion (P=10-10). Variation at 17q21.31 is associated with neurological diseases, and our collaboration is the first to report an association with EOC susceptibility. An integrated molecular analysis in this region provides evidence for ARHGAP27 and PLEKHM1 as candidate EOC susceptibility genes. © 2013 Macmillan Publishers Limited. All rights reserved.

Published
2013

18. GWAS meta-analysis and replication identifies three new susceptibility loci for ovarian cancer

Author

Pharoah, PDP, Tsai, YY, Ramus, SJ, Phelan, CM, Goode, EL, Lawrenson, K, Buckley, M, Fridley, BL, Tyrer, JP, Shen, H, Weber, R, Karevan, R, Larson, MC, Song, H, Tessier, DC, Bacot, F, Vincent, D, Cunningham, JM, Dennis, J, Dicks, E, Aben, KK, Anton-Culver, H, Antonenkova, N, Armasu, SM, Baglietto, L, Bandera, EV, Beckmann, MW, Birrer, MJ, Bloom, G, Bogdanova, N, Brenton, JD, Brinton, LA, Brooks-Wilson, A, Brown, R, Butzow, R, Campbell, I, Carney, ME, Carvalho, RS, Chang-Claude, J, Chen, YA, Chen, Z, Chow, WH, Cicek, MS, Coetzee, G, Cook, LS, Cramer, DW, Cybulski, C, Dansonka-Mieszkowska, A, Despierre, E, Doherty, JA, Dörk, T, Du Bois, A, Dürst, M, Eccles, D, Edwards, R, Ekici, AB, Fasching, PA, Fenstermacher, D, Flanagan, J, Gao, YT, Garcia-Closas, M, Gentry-Maharaj, A, Giles, G, Gjyshi, A, Gore, M, Gronwald, J, Guo, Q, Halle, MK, Harter, P, Hein, A, Heitz, F, Hillemanns, P, Hoatlin, M, Høgdall, E, Høgdall, CK, Hosono, S, Jakubowska, A, Jensen, A, Kalli, KR, and Karlan, BY

Subjects
endocrine system diseases
Abstract

Genome-wide association studies (GWAS) have identified four susceptibility loci for epithelial ovarian cancer (EOC), with another two suggestive loci reaching near genome-wide significance. We pooled data from a GWAS conducted in North America with another GWAS from the UK. We selected the top 24,551 SNPs for inclusion on the iCOGS custom genotyping array. We performed follow-up genotyping in 18,174 individuals with EOC (cases) and 26,134 controls from 43 studies from the Ovarian Cancer Association Consortium. We validated the two loci at 3q25 and 17q21 that were previously found to have associations close to genome-wide significance and identified three loci newly associated with risk: two loci associated with all EOC subtypes at 8q21 (rs11782652, P = 5.5 × 10-9) and 10p12 (rs1243180, P = 1.8 × 10-8) and another locus specific to the serous subtype at 17q12 (rs757210, P = 8.1 × 10-10). An integrated molecular analysis of genes and regulatory regions at these loci provided evidence for functional mechanisms underlying susceptibility and implicated CHMP4C in the pathogenesis of ovarian cancer.

Published
2013

19. Menarche, menopause, and breast cancer risk: individual participant meta-analysis, including 118 964 women with breast cancer from 117 epidemiological studies

Author

Beral, V, Bull, D, Pirie, K, Reeves, G, Peto, R, Skegg, D, LaVecchia, C, Magnusson, C, Pike, MC, Thomas, D, Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Friedenreich, CM, Calle, EE, Gapstur, SM, Patel, AV, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Marcou, Y, Kakouri, E, Duffy, SW, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Coogan, PF, Palmer, JR, Rosenberg, L, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Cummings, SR, Canfell, K, Sitas, F, Chao, P, Lissowska, J, Horn-Ross, PL, John, EM, Kolonel, LM, Nomura, AMY, Ghiasvand, R, Hu, J, Johnson, KC, Mao, Y, Callaghan, K, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Lindgard, I, Liu, B, Collins, R, Doll, R, Bishop, T, Fentiman, IS, De Sanjose, S, Gonzaler, CA, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wingo, P, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Eliassen, H, Gajalakshmi, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Neugut, A, Santella, R, Baines, CJ, Kreiger, N, Miller, AB, Wall, C, Tjonneland, A, Jorgensen, T, Stahlberg, C, Pedersen, AT, Flesch-Janys, D, Hakansson, N, Cauley, J, Heuch, I, Adami, HO, Persson, I, Weiderpass, E, Chang-Claude, J, Kaaks, R, McCredie, M, Paul, C, Skegg, DCG, Spears, GFS, Iwasaki, M, Tsugane, S, Anderson, G, Daling, JR, Hampton, J, Hutchinson, WB, Li, CI, Malone, K, Mandelson, M, Newcomb, P, Noonan, EA, Ray, RM, Stanford, JL, Tang, MTC, Thomas, DB, Weiss, NS, White, E, Izquierdo, A, Viladiu, P, Fourkala, EO, Jacobs, I, Menon, U, Ryan, A, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabal, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Riboli, E, Andrieu, N, Bachelot, A, Le, MG, Bremond, A, Gairard, B, Lansac, J, Piana, L, Renaud, R, Clavel-Chapelon, F, Fournier, A, Touillaud, M, Mesrine, S, Chabbert-Buffet, N, Boutron-Ruault, MC, Wolk, A, Torres-Mejia, G, Franceschi, S, Romieu, I, Boyle, P, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Ekbom, A, Erlandsson, G, Beeson, WL, Fraser, G, Peto, J, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Hartman, ML, Olsson, H, Goldbohm, RA, van den Brandt, PA, Palli, D, Teitelbaum, S, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Freedman, M, Hoover, R, Schairer, C, Ziegler, R, Banks, E, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, Graff-Iversen, S, Selmer, R, Jones, L, McPherson, K, Neil, A, Vessey, M, Yeates, D, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, McCann, SE, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, J-M, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Booth, JC, Jelihovsky, T, MacLennan, R, Shearman, R, Hadjisavvas, A, Kyriacou, K, Loisidou, M, Zhou, X, Wang, Q-S, Kawai, M, Minami, Y, Tsuji, I, Lund, E, Kumle, M, Stalsberg, H, Shu, XO, Zheng, W, Monninkhof, EM, Onland-Moret, NC, Peeters, PHM, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Tzonou, A, Baltzell, KA, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Gammon, MD, Hulka, BS, Millikan, R, Chilvers, CED, Lumachi, F, Bain, C, Schofield, F, Siskind, V, Rebbeck, TR, Bernstein, LR, Enger, S, Haile, RW, Paganini-Hill, A, Ross, RK, Ursin, G, Wu, AH, Yu, MC, Ewertz, DM, Clarke, EA, Bergkvist, L, Anderson, GL, Gass, M, O'Sullivan, MJ, Kalache, A, Farley, TMM, Holck, S, Meirik, O, Fukao, A, Factors, CGH, Grp, SHNHSIIIR, Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, RS: GROW - School for Oncology and Reproduction, RS: GROW - R1 - Prevention, RS: CAPHRI - R5 - Optimising Patient Care, and Collaborative Group on Hormonal Factors in Breast Cancer

Subjects
Aging, Breast cancer, Risk factors, Menopause, Menarche, cancer, malignancy, Ethnic origin, Disease, 0302 clinical medicine, Breast cancer, Risk Factors, Neoplasms, Receptors, Epidemiology, 80 and over, 030212 general & internal medicine, skin and connective tissue diseases, Aged, 80 and over, Patient, Obstetrics, Reproduction, Smoking, Age Factors, Middle Aged, Reproducibility, 3. Good health, Menopause, Receptors, Estrogen, Oncology, 030220 oncology & carcinogenesis, Menarche, Hormonal therapy, Female, epidemiology, Cancer Type - Breast Cancer, history, Adult, Risk, trends, medicine.medical_specialty, Design, Neoplasms, Hormone-Dependent, Requiring prolonged observation, Hormone Replacement Therapy, Oncology and Carcinogenesis, Breast Neoplasms, and over, Validity, methods, 03 medical and health sciences, Age, Clinical Research, Breast Cancer, medicine, Humans, cancer, Neoplasm Invasiveness, Women, Oncology & Carcinogenesis, Hormone-Dependent, breast, Aged, Gynecology, Collaborative Group on Hormonal Factors in Breast Cancer, therapy, business.industry, Contraception/Reproduction, Research, Estrogens, Etiology - Resources and Infrastructure, medicine.disease, Estrogen, Good Health and Well Being, cessation, Premenopause, Risk factors, Relative risk, Recall, business, malignancy, Meta-Analysis
Abstract

Background Menarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women.Methods Individual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression.Findings Breast cancer risk increased by a factor of 1.050 (95% CI 1.044-1.057; p < 0.0001) for every year younger at menarche, and independently by a smaller amount (1.029, 1.025-1.032; p < 0.0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1.43, 1.33-1.52, p < 0.001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p < 0.006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p < 0.01 for both comparisons).Interpretation The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.Funding Cancer Research UK.

Published
2012

20. Birth size and breast cancer risk: re-analysis of individual participant data from 32 studies

Author

Silva, IS, De Stavola, B, McCormack, V, Leon, D, Macintyre, S, Hodgson, ME, Newman, B, Sorensen, TIA, Olsen, LW, Baker, JL, Baron, JA, Newcomb, PA, Titus-Ernstoff, L, Egan, KM, Trentham-Dietz, A, Carbone, PP, Melleemkjaer, L, Sorensen, HT, Sandhu, MS, Bingham, S, Khaw, KT, Hilakivi-Clarke, L, Eriksson, J, Osmond, C, Lahmann, PH, Berglund, G, Kuh, D, Hardy, R, Mishra, G, Troisi, R, Palmer, J, Hatch, EE, Innes, K, Michels, KM, Park, SK, Brinton, LA, Garcia-Closas, M, Lissowska, J, Lissner, L, Hulthen, L, Sanderson, M, Malone, K, Daling, J, Stanford, J, Zheng, W, Shu, XO, Vatten, LJ, Nilsen, TIL, Ekbom, A, Kaijser, M, Cnattingius, S, Cade, JE, Burley, VJ, Greenwood, DC, Koupil, I, Freudenheim, JL, Nie, J, Liff, JM, and Christensen, D

Abstract

BACKGROUND: Birth size, perhaps a proxy for prenatal environment, might be a correlate of subsequent breast cancer risk, but findings from epidemiological studies have been inconsistent. We re-analysed individual participant data from published and unpublished studies to obtain more precise estimates of the magnitude and shape of the birth size-breast cancer association. METHODS AND FINDINGS: Studies were identified through computer-assisted and manual searches, and personal communication with investigators. Individual participant data from 32 studies, comprising 22,058 breast cancer cases, were obtained. Random effect models were used, if appropriate, to combine study-specific estimates of effect. Birth weight was positively associated with breast cancer risk in studies based on birth records (pooled relative risk [RR] per one standard deviation [SD] [= 0.5 kg] increment in birth weight: 1.06; 95% confidence interval [CI] 1.02-1.09) and parental recall when the participants were children (1.02; 95% CI 0.99-1.05), but not in those based on adult self-reports, or maternal recall during the woman's adulthood (0.98; 95% CI 0.95-1.01) (p for heterogeneity between data sources = 0.003). Relative to women who weighed 3.000-3.499 kg, the risk was 0.96 (CI 0.80-1.16) in those who weighed < 2.500 kg, and 1.12 (95% CI 1.00-1.25) in those who weighed > or = 4.000 kg (p for linear trend = 0.001) in birth record data. Birth length and head circumference from birth records were also positively associated with breast cancer risk (pooled RR per one SD increment: 1.06 [95% CI 1.03-1.10] and 1.09 [95% CI 1.03-1.15], respectively). Simultaneous adjustment for these three birth size variables showed that length was the strongest independent predictor of risk. The birth size effects did not appear to be confounded or mediated by established breast cancer risk factors and were not modified by age or menopausal status. The cumulative incidence of breast cancer per 100 women by age 80 y in the study populations was estimated to be 10.0, 10.0, 10.4, and 11.5 in those who were, respectively, in the bottom, second, third, and top fourths of the birth length distribution. CONCLUSIONS: This pooled analysis of individual participant data is consistent with birth size, and in particular birth length, being an independent correlate of breast cancer risk in adulthood

Published
2008

21. Breast cancer and hormonal contraceptives: Collaborative reanalysis of individual data on 53297 women with breast cancer and 100239 women without breast cancer from 54 epidemiological studies

Author

Calle, Ee, Heath, Cw, Miraclemcmahill, Hl, Coates, Rj, Liff, Jm, Franceschi, S., Talamini, R., Chantarakul, N., Koetsawang, S., Rachawat, D., Morabia, A., Schuman, L., Stewart, W., Szklo, M., Bain, C., Schofield, F., Siskind, V., Band, P., Coldman, Aj, Gallagher, Rp, Hislop, Tg, Yang, P., Duffy, Sw, Kolonel, Lm, Nomura, Amy, Oberle, Mw, Ory, Hw, Peterson, Hb, Wilson, Hg, Wingo, Pa, Ebeling, K., Kunde, D., Nishan, P., Graham Colditz, Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Mcmichael, Aj, Rohan, T., Ewertz, M., Paul, C., Skegg, Dcg, Boyle, P., Evstifeeva, M., Daling, Jr, Malone, K., Noonan, Ea, Stanford, Jl, Thomas, Db, Weiss, Ns, White, E., Andrieu, N., Bremond, A., Clavel, F., Gairard, B., Lansac, J., Piana, L., Renaud, R., Cuevas, Hr, Ontiveros, P., Palet, A., Salazar, Sb, Aristizabel, N., Cuadros, A., Bachelot, A., Le, Mg, Deacon, J., Peto, J., Taylor, Cn, Alfandary, E., Modan, B., Ron, E., Friedman, Gd, Hiatt, Ra, Bishop, T., Kosmelj, J., Primiczakelj, M., Ravnihar, B., Stare, J., Beeson, Wl, Fraser, G., Allen, Ds, Bulbrook, Rd, Cuzick, J., Fentiman, Is, Hayward, Jl, Wang, Dy, Hanson, Rl, Leske, Mc, Mahoney, Mc, Nasca, Pc, Varma, Ao, Weinstein, Al, Moller, Tr, Olsson, H., Ranstam, J., Goldbohm, Ra, Vandenbrandt, Pa, Apelo, Ra, Baens, J., Delacruz, Jr, Javier, B., Lacaya, Lb, Ngelangel, Ca, Lavecchia, C., Negri, E., Marubini, E., Ferraroni, M., Gerber, M., Richardson, S., Segala, C., Gatei, D., Kenya, P., Kungu, A., Mati, Jg, Brinton, La, Hoover, R., Schairer, C., Spirtas, R., Lee, Hp, Rookus, Ma, Vanleeuwen, Fe, Schoenberg, Ja, Gammon, Md, Clarke, Ea, Jones, L., Mcpherson, K., Neil, A., Vessey, M., Yeates, D., Beral, V., Bull, D., Crossley, B., Hermon, C., Jones, S., Key, T., Lewis, C., Reeves, G., Smith, P., Collins, R., Doll, R., Peto, R., Hannaford, P., Kay, C., Roserobixby, L., Gao, Yt, Yuan, Jm, Wei, Hy, Yun, T., Zhiheng, C., Berry, G., Booth, Jc, Jelihovsky, T., Maclennan, R., Shearman, R., Wang, Qs, Baines, Cj, Miller, Ab, Wall, C., Lund, E., Stalsberg, H., Dabancens, A., Martinez, L., Molina, R., Salas, O., Alexander, Fe, Hulka, Bs, Bernstein, L., Haile, Rw, Paganinihill, A., Pike, Mc, Ross, Rk, Ursin, G., Yu, Mc, Adami, Ho, Bergstrom, R., Longnecker, Mp, Newcomb, P., Farley, Tmn, Holck, S., Meirik, O., Calle EE, Heath CW, MiracleMcMahill HL, Coates RJ, Liff JM, Franceschi S, Talamini R, Chantarakul N, Koetsawang S, Rachawat D, Morabia A, Schuman L, Stewart W, Szklo M, Bain C, Schofield F, Siskind V, Band P, Coldman AJ, Gallagher RP, Hislop TG, Yang P, Duffy SW, Kolonel LM, Nomura AMY, Oberle MW, Ory HW, Peterson HB, Wilson HG, Wingo PA, Ebeling K, Kunde D, Nishan P, Colditz G, Martin N, Pardthaisong T, Silpisornkosol S, Theetranont C, Boosiri B, Chutivongse S, Jimakorn P, Virutamasen P, Wongsrichanalai C, McMichael AJ, Rohan T, Ewertz M, Paul C, Skegg DCG, Boyle P, Evstifeeva M, Daling JR, Malone K, Noonan EA, Stanford JL, Thomas DB, Weiss NS, White E, Andrieu N, Bremond A, Clavel F, Gairard B, Lansac J, Piana L, Renaud R, Cuevas HR, Ontiveros P, Palet A, Salazar SB, Aristizabel N, Cuadros A, Bachelot A, Le MG, Deacon J, Peto J, Taylor CN, Alfandary E, Modan B, Ron E, Friedman GD, Hiatt RA, Bishop T, Kosmelj J, PrimicZakelj M, Ravnihar B, Stare J, Beeson WL, Fraser G, Allen DS, Bulbrook RD, Cuzick J, Fentiman IS, Hayward JL, Wang DY, Hanson RL, Leske MC, Mahoney MC, Nasca PC, Varma AO, Weinstein AL, Moller TR, Olsson H, Ranstam J, Goldbohm RA, vandenBrandt PA, Apelo RA, Baens J, delaCruz JR, Javier B, Lacaya LB, Ngelangel CA, LaVecchia C, Negri E, Marubini E, Ferraroni M, Gerber M, Richardson S, Segala C, Gatei D, Kenya P, Kungu A, Mati JG, Brinton LA, Hoover R, Schairer C, Spirtas R, Lee HP, Rookus MA, vanLeeuwen FE, Schoenberg JA, Gammon MD, Clarke EA, Jones L, McPherson K, Neil A, Vessey M, Yeates D, Beral V, Bull D, Crossley B, Hermon C, Jones S, Key T, Lewis C, Reeves G, Smith P, Collins R, Doll R, Peto R, Hannaford P, Kay C, RoseroBixby L, Gao YT, Yuan JM, Wei HY, Yun T, Zhiheng C, Berry G, Booth JC, Jelihovsky T, MacLennan R, Shearman R, Wang QS, Baines CJ, Miller AB, Wall C, Lund E, Stalsberg H, Dabancens A, Martinez L, Molina R, Salas O, Alexander FE, Hulka BS, Bernstein L, Haile RW, PaganiniHill A, Pike MC, Ross RK, Ursin G, Yu MC, Adami HO, Bergstrom R, Longnecker MP, Newcomb P, Farley TMN, Holck S, and Meirik O

Abstract

Background The Collaborative Group on Hormonal Factors in Breast Cancer has brought together and reanalysed the worldwide epidemiological evidence on the relation between breast cancer risk and use of hormonal contraceptives. Methods Individual data on 53297 women with breast cancer and 100 239 women without breast cancer from 54 studies conducted in 25 countries were collected, checked, and analysed centrally. Estimates of the relative risk for breast cancer were obtained by a modification of the Mantel-Haenszel method. All analyses were stratified by study, age at diagnosis, parity, and, where appropriate, the age a woman was when her first child was born, and the age she was when her risk of conception ceased. Findings The results provide strong evidence for two main conclusions. First, while women are taking combined oral contraceptives and in the 10 years after stopping there is a small increase in the relative risk of having breast cancer diagnosed (relative risk [95% CI] in current users 1.24 [1.15-1.33], 2p

Published
1996

22. Breast cancer and hormonal contraceptives: Further results

Author

Calle, Ee, Heath, Cw, Miraclemcmahill, Hl, Coates, Rj, Liff, Jm, Franceschi, S., Talamini, R., Chantarakul, N., Koetsawang, S., Rachawat, D., Morabia, A., Schuman, I., Stewart, W., Szklo, M., Bain, C., Schofield, F., Siskind, V., Band, P., Coldman, Aj, Gallagher, Rp, Hislop, Tg, Yang, P., Duffy, Sw, Kolonel, Lm, Nomura, Amy, Oberle, Mw, Ory, Hw, Peterson, Hb, Wilson, Hg, Wingo, Pa, Ebeling, K., Kunde, D., Nishan, P., Colditz, G., Martin, N., Pardthaisong, T., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Mcmichael, Aj, Rohan, T., Ewertz, M., Paul, C., Skegg, Dcg, Spears, Gfs, Boyle, P., Evstifeeva, T., Daling, Jr, Malone, K., Noonan, Ea, Stanford, Jl, Thomas, Db, Weiss, Ns, White, E., Andrieu, N., Bremond, A., Clavel, F., Gairard, B., Lansac, J., Piana, L., Renaud, R., Fine, Srp, Cuevas, Hr, Ontiveros, P., Palet, A., Salazar, Sb, Aristizabel, N., Cuadros, A., Bachelot, A., Le, Mg, Deacon, J., Peto, J., Taylor, Cn, Alfandary, E., Modan, B., Ron, E., Friedman, Gd, Hiatt, Ra, Bishop, T., Kosmelj, K., Primiczakelj, M., Ravnihar, B., Stare, J., Beeson, Wl, Fraser, G., Allen, Ds, Bulbrook, Rd, Cuzick, J., Fentiman, Is, Hayward, Jl, Wang, Dy, Hanson, Rl, Leske, Mc, Mahoney, Mc, Nasca, Pc, Varma, Ap, Weinstein, Al, Moller, Tr, Olsson, H., Ranstam, J., Goldbohm, Ra, Vandenbrandt, Pa, Apelo, Ra, Baens, J., Delacruz, Jr, Javier, B., Lacaya, Lb, Ngelangel, Ca, Lavecchia, C., Eva Negri, Marbuni, E., Ferraroni, M., Gerber, M., Richardson, S., Segala, C., Gatei, D., Kenya, P., Kungu, A., Mati, Jg, Brinton, La, Hoover, R., Schairer, C., Spirtas, R., Lee, Hp, Rookus, Ma, Vanleeuwen, Fe, Schoenberg, Ja, Gammon, Md, Clarke, Ea, Jones, L., Mcpherson, K., Neil, A., Vessey, M., Yeates, D., Beral, V., Bull, D., Crossley, B., Hermon, C., Jones, S., Key, T., Lewis, C., Reeves, G., Smith, P., Collins, R., Doll, R., Peto, R., Hannaford, P., Kay, C., Roserobixby, L., Yuan, Jm, Wei, Hy, Yun, T., Zhiheng, C., Berry, G., Booth, Jc, Jelihovsky, T., Maclennan, R., Shearman, R., Wang, Qs, Baines, Cj, Miller, Ab, Wall, C., Lund, E., Stalsberg, H., Dabancens, A., Martinez, L., Molina, R., Salas, O., Alexander, Fe, Hulka, Bs, Chilvers, Ced, Bernstein, L., Haile, Rw, Paganinihill, A., Pike, Mc, Ross, Rk, Ursin, G., Yu, Mc, Adami, Ho, Bergstrom, R., Longnecker, Mp, Newcomb, P., Farley, Tmn, Holck, S., Meirik, O., Calle EE, Heath CW, MiracleMcMahill HL, Coates RJ, Liff JM, Franceschi S, Talamini R, Chantarakul N, Koetsawang S, Rachawat D, Morabia A, Schuman I, Stewart W, Szklo M, Bain C, Schofield F, Siskind V, Band P, Coldman AJ, Gallagher RP, Hislop TG, Yang P, Duffy SW, Kolonel LM, Nomura AMY, Oberle MW, Ory HW, Peterson HB, Wilson HG, Wingo PA, Ebeling K, Kunde D, Nishan P, Colditz G, Martin N, Pardthaisong T, Silpisornkosol S, Theetranont C, Boosiri B, Chutivongse S, Jimakorn P, Virutamasen P, Wongsrichanalai C, McMichael AJ, Rohan T, Ewertz M, Paul C, Skegg DCG, Spears GFS, Boyle P, Evstifeeva T, Daling JR, Malone K, Noonan EA, Stanford JL, Thomas DB, Weiss NS, White E, Andrieu N, Bremond A, Clavel F, Gairard B, Lansac J, Piana L, Renaud R, Fine SRP, Cuevas HR, Ontiveros P, Palet A, Salazar SB, Aristizabel N, Cuadros A, Bachelot A, Le MG, Deacon J, Peto J, Taylor CN, Alfandary E, Modan B, Ron E, Friedman GD, Hiatt RA, Bishop T, Kosmelj K, PrimicZakelj M, Ravnihar B, Stare J, Beeson WL, Fraser G, Allen DS, Bulbrook RD, Cuzick J, Fentiman IS, Hayward JL, Wang DY, Hanson RL, Leske MC, Mahoney MC, Nasca PC, Varma AP, Weinstein AL, Moller TR, Olsson H, Ranstam J, Goldbohm RA, vandenBrandt PA, Apelo RA, Baens J, delaCruz JR, Javier B, Lacaya LB, Ngelangel CA, LaVecchia C, Negri E, Marbuni E, Ferraroni M, Gerber M, Richardson S, Segala C, Gatei D, Kenya P, Kungu A, Mati JG, Brinton LA, Hoover R, Schairer C, Spirtas R, Lee HP, Rookus MA, vanLeeuwen FE, Schoenberg JA, Gammon MD, Clarke EA, Jones L, McPherson K, Neil A, Vessey M, Yeates D, Beral V, Bull D, Crossley B, Hermon C, Jones S, Key T, Lewis C, Reeves G, Smith P, Collins R, Doll R, Peto R, Hannaford P, Kay C, RoseroBixby L, Yuan JM, Wei HY, Yun T, Zhiheng C, Berry G, Booth JC, Jelihovsky T, MacLennan R, Shearman R, Wang QS, Baines CJ, Miller AB, Wall C, Lund E, Stalsberg H, Dabancens A, Martinez L, Molina R, Salas O, Alexander FE, Hulka BS, Chilvers CED, Bernstein L, Haile RW, PaganiniHill A, Pike MC, Ross RK, Ursin G, Yu MC, Adami HO, Bergstrom R, Longnecker MP, Newcomb P, Farley TMN, Holck S, and Meirik O

Abstract

The Collaborative Group on Hormonal Factors in Breast Cancer has brought together and reanalysed the worldwide epidemiological evidence on breast cancer risk and use oi hormonal contraceptives. Original data from 54 studies, representing about 90% of the information available on the topic, were collected, checked and analysed centrally. The 54 studies were performed in 26 countries and include a total of 53,297 women with breast cancer and 100,239 women without breast cancer. The studies were varied in their design, setting and timing. Most information came from case-control studies with controls chosen from the general population; most women resided in Europe or North America and most cancers were diagnosed during the 1980s. Overall 41% of the women with breast cancer and 40% of the women without breast cancer had used oral contraceptives at some time: the median age at first use was 26 years, the median duration of use was 3 years, the median year of first use was 1968, the median time since first use was 16 years, and the median time since last use was 9 years. The main findings, summarised elsewhere,I are that there is a small increase in the risk of having breast cancer diagnosed in current users of combined oral contraceptives and in women who had stopped use in the past 10 years but that there is no evidence of an increase in the risk more than 10 years after stopping use. In addition, the cancers diagnosed in women who had used oral contraceptives tended to be less advanced clinically than the cancers diagnosed in women who had not used them. Despite the large number of possibilities investigated, few factors appeared to modify the main findings either in recent or in past users. For recent users who began use before age 20 the relative risks are higher than for recent users who began at older ages. For women whose use of oral contraceptives ceased more than 10 years before there was some suggestion of a reduction in breast cancer risk in certain subgroups, with a deficit of tumors that had spread beyond the breast, especially among women who had used preparations containing the highest doses of oestrogen and progestogen. These findings are unexpected and need to be confirmed. Although these data represent most of the epidemiologi cal evidence on the topic to date, there is still insufficient information to comment reliably about the effects of specific types of oestrogen or of progestogen. What evidence there is suggests, however, no major differences in the effects for specific types of oestrogen or of progestogen and that the pattern of risk associated with use of hormonal contraceptives containing progestogens alone may be similar to that observed for preparations containing both oestrogens and progestogens. On the basis of these results, there is little difference between women who have and have not used combined oral contraceptives in terms of the estimated cumulative number of breast cancers diagnosed during the period from starting use up to 20 rears after stopping. The cancers diagnosed in women who have used oral contraceptives are, however, less advanced clinically than the cancers diag nosed in never users. Further research is needed to establish whether the associations described here are due to earlier diagnosis of breast cancer in women who have used oral contraceptives, to the biological effects of the hormonal contraceptives or to a combination of both. Little information is as yet available about the effects on breast cancer risk of oral contraceptive use that ceased more than 20 years before and as such data accumulate it will be necessary to reexamine the worldwide evidence. RI Ranstam, Jonas/A-4386-2009; Colditz, Graham/A-3963-2009

Published
1996

23. Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58515 women with breast cancer and 95067 women without the disease

Author

Beral, V Hamajima, N Hirose, K Rohan, T Calle, EE and Heath, CW Coates, RJ Liff, JM Talamini, R Chantarakul, N and Koetsawang, S Rachawat, D Morabia, A Schuman, L and Stewart, W Szklo, M Bain, C Schofield, F Siskind, V and Band, P Coldman, AJ Gallagher, RP Hislop, TG Yang, P and Kolonel, LM Nomura, AMY Hu, J Johnson, KC Mao, Y De Sanjose, S Lee, N Marchbanks, P Ory, HW Peterson, HB and Wilson, HG Wingo, PA Ebeling, K Kunde, D Nishan, P and Hopper, JL Colditz, G Gajalakshmi, V Martin, N and Pardthaisong, T Solpisornkosol, S Theetranont, C Boosiri, B and Chutivongse, S Jimakorn, P Virutamasen, P and Wongsrichanalai, C Ewertz, M Adami, HO Bergkvist, L and Magnusson, C Persson, I Chang-Claude, J Paul, C Skegg, DCG Spears, GFS Boyle, P Evstifeeva, T Daling, JR and Hutchinson, WB Malone, K Noonan, EA Stanford, JL Thomas, DB Weiss, NS White, E Andrieu, N Bremond, A Clavel, F Gairard, B Lansac, J Piana, L Renaud, R Izquierdo, A Viladiu, P Cuevas, HR Ontiveros, P Palet, A and Salazar, SB Arsitizabal, N Cuadros, A Tryggvadottir, L and Tulinius, H Bachelot, A Le, MG Peto, J Franceschi, S and Lubin, F Modan, B Ron, E Wax, Y Friedman, GD Hiatt, RA Levi, F Bishop, T Kosmelj, K Primic-Zakelj, M and Ravnihar, B Stare, J Beeson, WL Fraser, G Bulbrook, RD and Cuzick, J Duffy, SW Fentiman, IS Hayward, JL Wang, DY McMichael, AJ McPherson, K Hanson, RL Leske, MC and Mahoney, MC Nasca, PC Varma, AO Weinstein, AL Moller, TR and Olsson, H Ranstam, J Goldbohm, RA van den Brandt, PA and Apelo, RA Baens, J de la Cruz, JR Javier, B Lacaya, LB and Ngelangel, CA La Vecchia, C Negri, E Marubini, E and Ferraroni, M Gerber, M Richardson, S Segala, C Gatei, D and Kenya, P Kungu, A Mati, JG Brinton, LA Hoover, R and Schairer, C Spirtas, R Lee, HP Rookus, MA van Leeuwen, FE Schoenberg, JA McCredie, M Gammon, MD Clarke, EA and Jones, L Neil, A Vessey, M Yeates, D Appleby, P and Banks, E Bull, D Crossley, B Goodill, A Green, J and Hermon, C Key, T Langston, N Lewis, C Reeves, G and Collins, R Doll, R Peto, R Mabuchi, K Preston, D and Hannaford, P Kay, C Rosero-Bixby, L Gao, YT Jin, F and Yuan, JM Wei, HY Yun, T Zhiheng, C Berry, G Cooper Booth, J Jelihovsky, T MacLennan, R Shearman, R Wang, QS and Baines, CJ Miller, AB Wall, C Lund, E Stalsberg, H and Shu, XO Zheng, W Katsouyanni, K Trichopoulou, A and Trichopoulos, D Dabancens, A Martinez, L Molina, R and Salas, O Alexander, XE Anderson, K Folsom, AR Hulka, BS and Bernstein, L Enger, S Haile, RW Paganini-Hill, A and Pike, MC Ross, RK Ursin, G Yu, MC Longnecker, MP and Newcomb, P Bergkvist, L Kalache, A Farley, TMM Holck, S and Meirik, O Collaborative Group on Hormonal Factors in Breast Cancer

Abstract

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women’s age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P

Published
2002

27. Abstract P3-12-05: Genetic Variation in Prolactin and Prolactin Receptor, and Relationships with Serum Prolactin Levels and Breast Cancer Risk

Author

Nyante, SJ, primary, Faupel-Badger, JM, additional, Sherman, ME, additional, Gaudet, MM, additional, Falk, RT, additional, Andaya, AA, additional, Pfeiffer, RM, additional, Lissowska, J, additional, Brinton, LA, additional, Peplonska, B, additional, Vonderhaar, BK, additional, Chanock, SJ, additional, Garcia-Closas, M, additional, and Figueroa, JD., additional

Published
2010
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28. Breast cancer and hormonal contraceptives: further results

Author

Calle, EE, primary, Heath, CW, additional, Miracle-McMahill, HL, additional, Coates, RJ, additional, Liff, JM, additional, Franceschi, S, additional, Talamini, R, additional, Chantarakul, N, additional, Koetsawang, S, additional, Rachawat, D, additional, Morabia, A, additional, Schuman, L, additional, Stewart, W, additional, Szklo, M, additional, Bain, C, additional, Schofield, F, additional, Siskind, V, additional, Band, P, additional, Coldman, AJ, additional, Gallagher, RP, additional, Hislop, TG, additional, Yang, P, additional, Duffy, SW, additional, Kolonel, LM, additional, Nomura, AMY, additional, Oberle, MW, additional, Ory, HW, additional, Peterson, HB, additional, Wilson, HG, additional, Wingo, PA, additional, Ebeling, K, additional, Kunde, D, additional, Nishan, P, additional, Colditz, G, additional, Martin, N, additional, Pardthaisong, T, additional, Silpisornkosol, S, additional, Theetranont, C, additional, Boosiri, B, additional, Chutivongse, S, additional, Jimakorn, P, additional, Virutamasen, P, additional, Wongsrichanalai, C, additional, McMichael, AJ, additional, Rohan, T, additional, Ewertz, M, additional, Paul, C, additional, Skegg, DCG, additional, Spears, GFS, additional, Boyle, P, additional, Evstifeeva, T, additional, Daling, JR, additional, Malone, K, additional, Noonan, EA, additional, Stanford, JL, additional, Thomas, DB, additional, Weiss, NS, additional, White, E, additional, Andrieu, N, additional, Brêmond, A, additional, Clavel, F, additional, Gairard, B, additional, Lansac, J, additional, Piana, L, additional, Renaud, R, additional, Fine, SRP, additional, Cuevas, HR, additional, Ontiveros, P, additional, Palet, A, additional, Salazar, SB, additional, Aristizabel, N, additional, Cuadros, A, additional, Bachelot, A, additional, Leê, MG, additional, Deacon, J, additional, Peto, J, additional, Taylor, CN, additional, Alfandary, E, additional, Modan, B, additional, Ron, E, additional, Friedman, GD, additional, Hiatt, RA, additional, Bishop, T, additional, Kosmelj, K., additional, Primic-Zakelj, M, additional, Ravnihar, B, additional, Stare, J, additional, Beeson, WL, additional, Fraser, G, additional, Allen, DS, additional, Bulbrook, RD, additional, Cuzick, J, additional, Fentiman, IS, additional, Hayward, JL, additional, Wang, DY, additional, Hanson, RL, additional, Leske, MC, additional, Mahoney, MC, additional, Nasca, PC, additional, Varma, AO, additional, Weinstein, AL, additional, Moller, TR, additional, Olsson, H, additional, Ranstam, J, additional, Goldbohm, RA, additional, van den Brandt, PA, additional, Apelo, RA, additional, Baens, J, additional, de la Cruz, JR, additional, Javier, B, additional, Lacaya, LB, additional, Ngelangel, CA, additional, La Vecchia, C, additional, Negri, E, additional, Marbuni, E, additional, Ferraroni, M, additional, Gerber, M, additional, Richardson, S, additional, Segala, C, additional, Gatei, D, additional, Kenya, P, additional, Kungu, A, additional, Mati, JG, additional, Brinton, LA, additional, Hoover, R, additional, Schairer, C, additional, Spirtas, R, additional, Lee, HP, additional, Rookus, MA, additional, van Leeuwen, FE, additional, Schoenberg, JA, additional, Gammon, MD, additional, Clarke, EA, additional, Jones, L, additional, McPherson, K, additional, Neil, A, additional, Vessey, M, additional, Yeates, D., additional, Beral, V, additional, Bull, D, additional, Crossley, B, additional, Hermon, C, additional, Jones, S, additional, Key, T, additional, Reeves, Clewis G, additional, Smith, P, additional, Collins, R, additional, Doll, R, additional, Peto, R, additional, Hannaford, P, additional, Kay, C, additional, Rosero-Bixby, L, additional, Yuan, J-M, additional, Wei, HY, additional, Yun, T, additional, Zhiheng, C, additional, Berry, G, additional, Booth, J Cooper, additional, Jelihovsky, T, additional, Maclennan, R, additional, Shearman, R, additional, Wang, Q-S, additional, Baines, CJ, additional, Miller, AB, additional, Wall, C, additional, Lund, E, additional, Stalsberg, H, additional, Dabancens, A, additional, Martinez, L, additional, Molina, R, additional, Salas, O, additional, Alexander, FE, additional, Hulka, BS, additional, Chilvers, CED, additional, Bernstein, L, additional, Haile, RW, additional, Paganini-Hill, A, additional, Pike, MC, additional, Ross, RK, additional, Ursin, G, additional, Yu, MC, additional, Adami, HO, additional, Bergstrom, R, additional, Longnecker, MP, additional, Farley, TMN, additional, Holck, S, additional, and Meirik, O, additional

Published
1996
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32. Non-steroidal anti-inflammatory drug use and ovarian cancer risk: findings from the NIH-AARP Diet and Health Study and systematic review.

Author

Murphy MA, Trabert B, Yang HP, Park Y, Brinton LA, Hartge P, Sherman ME, Hollenbeck A, Wentzensen N, Murphy, Megan A, Trabert, Britton, Yang, Hannah P, Park, Yikyung, Brinton, Louise A, Hartge, Patricia, Sherman, Mark E, Hollenbeck, Albert, and Wentzensen, Nicolas

Abstract

Background: Chronic inflammation has been proposed as a risk factor for ovarian cancer. Some data suggest that anti-inflammatory medications may be protective against ovarian cancer; however, results have been inconsistent.Methods: We evaluated the risk of epithelial ovarian cancer with regular use of NSAIDs prospectively in the NIH-AARP Diet and Health Study, using Cox proportional hazard models. We also examined the risk of common subtypes of epithelial ovarian cancer (serous, mucinous, endometrioid, clear cell, and other epithelial) with regular use of NSAIDs. In addition, we performed meta-analyses summarizing the risk of ovarian cancer with "regular use" of NSAIDs in previously published studies.Results: We did not observe a significant association between regular use of NSAIDs with ovarian cancer risk in the AARP cohort (aspirin: RR 1.06, 95 % CI 0.87-1.29; non-aspirin NSAIDs: RR 0.93, 95 % CI 0.74-1.15); however, summary estimates from prospective cohort studies demonstrated that use of non-aspirin NSAIDs may reduce the risk of ovarian cancer (RR 0.88, 95 % CI 0.77-1.01). Although not significant, we found that mucinous tumors were inversely associated with non-aspirin NSAID use (RR 0.69, 95 % CI 0.23-2.10) in the AARP cohort, which was supported by the meta-analysis (RR 0.69, CI 0.50-0.94.)Conclusion: Although results from the NIH-AARP cohort study were not statistically significant, our meta-analysis suggests that non-aspirin NSAIDs may be protective against ovarian cancer. Additional analyses, focusing on dose, duration, and frequency of NSAID use and accounting for ovarian cancer heterogeneity are necessary to further elucidate the association between NSAID use and ovarian cancer risk. [ABSTRACT FROM AUTHOR]

Published
2012
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34. Relationship between mammographic density and breast cancer death in the Breast Cancer Surveillance Consortium.

Author

Gierach GL, Ichikawa L, Kerlikowske K, Brinton LA, Farhat GN, Vacek PM, Weaver DL, Schairer C, Taplin SH, Sherman ME, Gierach, Gretchen L, Ichikawa, Laura, Kerlikowske, Karla, Brinton, Louise A, Farhat, Ghada N, Vacek, Pamela M, Weaver, Donald L, Schairer, Catherine, Taplin, Stephen H, and Sherman, Mark E

Abstract

Background: Women with elevated mammographic density have an increased risk of developing breast cancer. However, among women diagnosed with breast cancer, it is unclear whether higher density portends reduced survival, independent of other factors.Methods: We evaluated relationships between mammographic density and risk of death from breast cancer and all causes within the US Breast Cancer Surveillance Consortium. We studied 9232 women diagnosed with primary invasive breast carcinoma during 1996-2005, with a mean follow-up of 6.6 years. Mammographic density was assessed using the Breast Imaging Reporting and Data System (BI-RADS) density classification. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated by Cox proportional hazards regression; women with scattered fibroglandular densities (BI-RADS 2) were the referent group. All statistical tests were two-sided.Results: A total of 1795 women died, of whom 889 died of breast cancer. In multivariable analyses (adjusted for site, age at and year of diagnosis, American Joint Committee on Cancer stage, body mass index, mode of detection, treatment, and income), high density (BI-RADS 4) was not related to risk of death from breast cancer (HR = 0.92, 95% CI = 0.71 to 1.19) or death from all causes (HR = 0.83, 95% CI = 0.68 to 1.02). Analyses stratified by stage and other prognostic factors yielded similar results, except for an increased risk of breast cancer death among women with low density (BI-RADS 1) who were either obese (HR = 2.02, 95% CI = 1.37 to 2.97) or had tumors of at least 2.0 cm (HR = 1.55, 95% CI = 1.14 to 2.09).Conclusions: High mammographic breast density was not associated with risk of death from breast cancer or death from any cause after accounting for other patient and tumor characteristics. Thus, risk factors for the development of breast cancer may not necessarily be the same as factors influencing the risk of death after breast cancer has developed. [ABSTRACT FROM AUTHOR]

Published
2012
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35. Active and passive cigarette smoking and the risk of endometrial cancer in Poland.

Author

Yang HP, Brinton LA, Platz EA, Lissowska J, Lacey JV Jr., Sherman ME, Peplonska B, and Garcia-Closas M

Abstract

BACKGROUND: Epidemiological studies have consistently reported that active cigarette smoking is inversely associated with endometrial cancer risk. However, dose-response relationships with quantitative measures of active smoking or passive smoking remain less clear. METHODS: Data on lifetime active and passive smoking were collected for 551 endometrial cancer cases and 1925 controls in a population-based case-control study conducted during 2001-2003 in Poland (Warsaw and ódz). RESULTS: Compared with never active smokers, active current (Odds Ratio (OR)=0.51, 95% Confidence Interval (CI): 0.39, 0.68) and former smokers (OR=0.60, 95% CI: 0.45, 0.80) were at a statistically significantly decreased risk. We did not observe statistically significant inverse dose-response relationships with increasing exposure with duration and cumulative measures. However, there was some indication that the highest category of number of years (OR=0.35, 95% CI: 0.23-0.55), intensity (OR=0.41, 95% CI: 0.24-0.69), and dose (OR=0.38, 95% CI: 0.24-0.60) of smoking among current smokers had the greatest inverse association compared to never smokers. Our data did not support the presence of an inverse association with passive smoking among never active smokers (OR=0.92; 95% CI: 0.65, 1.29). CONCLUSION: Our results support that long-term and heavy smoking among current smokers strongly influence endometrial cancer risk. [ABSTRACT FROM AUTHOR]

Published
2010
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36. Prospective case-control study of serum mullerian inhibiting substance and breast cancer risk.

Author

Dorgan JF, Stanczyk FZ, Egleston BL, Kahle LL, Shaw CM, Spittle CS, Godwin AK, Brinton LA, Dorgan, Joanne F, Stanczyk, Frank Z, Egleston, Brian L, Kahle, Lisa L, Shaw, Christiana M, Spittle, Cynthia S, Godwin, Andrew K, and Brinton, Louise A

Abstract

Background: Müllerian inhibiting substance (MIS) is a member of the transforming growth factor beta family of growth and differentiation factors that inhibits elongation and branching of mammary ducts and has been shown to inhibit mammary tumor growth in vitro and in animal models. The objective of this study was to determine whether serum MIS levels are associated with breast cancer risk.Methods: We conducted a prospective case-control study of 309 participants who were registered in the Columbia, Missouri Serum Bank. Each of 105 in situ or invasive breast cancer case patients with prediagnostic serum collected before menopause was matched to two control subjects by age, date, menstrual cycle day, and time of day of blood collection. MIS was measured in serum by using an enzyme-linked immunosorbent assay, and estradiol and testosterone concentrations were quantified by using specific radioimmunoassays. Data were analyzed using conditional logistic regression. All tests of statistical significance were two-sided.Results: The relative odds ratio of breast cancer for women in increasing MIS quartiles were 1, 2.8 (95% confidence interval [CI] = 1.0 to 7.4), 5.9 (95% CI = 2.4 to 14.6), and 9.8 (95% CI = 3.3 to 28.9, P(trend) < .001). The association of MIS with breast cancer was weaker in women who were not taking oral contraceptives at the time of blood collection, but adjustment for estradiol and testosterone levels did not materially alter results for these women. The association of MIS with breast cancer did not vary by age at blood collection but was stronger among women who were diagnosed with breast cancer at an older age than among those who were diagnosed at a younger age.Conclusion: MIS may be a novel biomarker of increased breast cancer risk. Additional research including confirmatory epidemiological studies and mechanistic studies is needed. [ABSTRACT FROM AUTHOR]

Published
2009
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37. Alcohol and risk of breast cancer by histologic type and hormone receptor status in postmenopausal women: the NIH-AARP Diet and Health Study.

Author

Lew JQ, Freedman ND, Leitzmann MF, Brinton LA, Hoover RN, Hollenbeck AR, Schatzkin A, and Park Y

Abstract

Little is known about the association between alcohol and breast cancer by different tumor characteristics. The study consisted of 184,418 postmenopausal women aged 50-71 years in the National Institutes of Health-AARP Diet and Health Study (1995-2003). Alcohol use, diet, and potential risk factors for cancer were assessed with a mailed questionnaire at baseline. The relative risks and 95% confidence intervals were estimated by using Cox proportional hazards regression. Breast cancer cases and estrogen receptor and progesterone receptor status were identified through linkage to state cancer registries. During an average of 7 years of follow-up, 5,461 breast cancer cases were identified. Alcohol was significantly positively associated with total breast cancer: Even a moderate amount of alcohol (>10 g/day) significantly increased breast cancer risk. In a comparison of >35 g versus 0 g/day, the multivariate relative risks were 1.35 (95% confidence interval (CI): 1.17, 1.56) for total breast cancer, 1.46 (95% CI: 1.22, 1.75) for ductal tumors, and 1.52 (95% CI: 0.95, 2.44) for lobular tumors. The multivariate relative risks for estrogen receptor-positive/progesterone receptor-positive, estrogen receptor-positive/progesterone receptor-negative, and estrogen receptor-negative/progesterone receptor-negative tumors were 1.46 (95% CI: 1.12, 1.91) for >35 g versus 0 g/day, 1.13 (95% CI: 0.73, 1.77) for >20 g versus 0 g/day, and 1.21 (95% CI: 0.79, 1.84) for >20 g versus 0 g/day, respectively. Moderate consumption of alcohol was associated with breast cancer, specifically hormone receptor-positive tumors. [ABSTRACT FROM AUTHOR]

Published
2009
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41. Characteristics associated with recent recreational exercise among women 20 to 44 years of age.

Author

Britton JA, Gammon MD, Kelsey JL, Brogan DJ, Coates RJ, Schoenberg JB, Potischman N, Swanson CA, Stanford JL, and Brinton LA

Abstract

Data on 1,501 control women from a multi-center, population-based, case-control study of breast cancer were used to examine characteristics associated with recreational exercise during the year prior to the interview among women 20 to 44 years of age. In a univariate analysis, higher levels of recreational exercise were associated with: higher education; higher family income; white race; previous participation in recreational exercise above the median level at ages 12 to 13 and at age 20; being nulliparous; ever lactating; being a never or past smoker; having a low current Quetelet's index (QI: weight in kilograms divided by height in meters squared); and living in Atlanta or Seattle (compared to New Jersey). 1n a multiple linear regression model, independent predictors of higher levels of recreational exercise were: participation in higher levels of exercise at 20 years of age; having a low current QI; and never having smoked. Though all women should be encouraged to participate in exercise, these findings identity subgroups of women that may need targeting when developing exercise intervention programs. [ABSTRACT FROM AUTHOR]

Published
2000

42. Breast cancer risk in young women and history of selected medical conditions.

Author

Weiss, HA, Brinton, LA, Potischman, NA, Brogan, D, Coates, RJ, Gammon, MD, Malone, KE, Schoenberg, JB, Weiss, H A, Brinton, L A, Potischman, N A, Coates, R J, Gammon, M D, Malone, K E, and Schoenberg, J B

Abstract

Background: Several common medical conditions are associated with altered hormone levels, and may thus plausibly influence breast cancer risk. Few studies have examined such relationships, and we utilized a population-based case-control study of young women in the US to examine breast cancer risk following a history of various medical conditions. Relationships between breast cancer and each medical condition examined are biologically plausible, and relevant in terms of public health.Methods: The study included 2173 breast cancer cases and 1990 population-based controls from three areas of the US, under 55 years, who were administered a questionnaire including details of physician-diagnosed medical conditions.Results: No significantly increased or decreased breast cancer risk was associated with a history of thyroid disease, gallbladder disease, colorectal polyps, diabetes, high blood pressure, high cholesterol or surgery for endometriosis. There was some evidence of an increased breast cancer risk associated with ovarian cysts among women who did not receive an oophorectomy (relative risk [RR] = 1.94, 95% CI: 1.0-3.9). Non-significant increases in breast cancer risk were observed following diagnoses of several other cancers, including thyroid cancer, basal cell carcinoma, Hodgkin's disease and malignant melanoma.Conclusions: To conclude, our generally null results from this large, population-based study support results from previous studies in providing reassurance that women with a history of several common medical conditions do not appear to be at an increased risk of breast cancer at a young age. [ABSTRACT FROM AUTHOR]

Published
1999
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43. Hip fractures among infertile women.

Author

Hesdorffer DC, Melton LJ III, Malkasian GD, Atkinson EJ, Brinton LA, and O'Fallon WM

Abstract

The relation of antioxidant nutrients to the incidence of nuclear cataracts was investigated in a cohort of adults aged 43-84 years in the Beaver Dam Eye Study (Beaver Dam, Wisconsin). Nuclear opacity was assessed on a five-point ordinal scale using lens photographs taken at baseline (1988-1990) and at follow-up (1993-1995). Of the 1,354 persons eligible, 246 developed a nuclear cataract (level 4 or 5 opacity) in at least one eye. Antioxidant intakes were assessed using a food frequency questionnaire administered at baseline for time points corresponding to intake during the year preceding baseline and 10 years before baseline (the distant past). Lutein-zeaxanthin was the only carotenoid, out of five examined, that was associated with nuclear cataracts. Persons in the highest quintile of lutein intake in the distant past were half as likely to have an incident cataract as persons in the lowest quintile of intake (95% confidence interval 0.3-0.8). In the overall group, nuclear cataracts were not significantly related to intake of vitamin C or vitamin E. However, vitamins C and E were inversely associated with opacities in persons who had some other risk factors for cataracts. While results of this short term follow-up study are consistent with a possible protective influence of lutein and vitamins E and C on the development of nuclear cataracts, the evidence in the present study provides weak support for these associations. [ABSTRACT FROM AUTHOR]

Published
1999
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44. Intrauterine device use and endometrial cancer risk.

Author

Sturgeon, SR, Brinton, LA, Berman, ML, Mortel, R, Twiggs, LB, Barrett, RJ, Wilbanks, GD, Lurain, JR, Sturgeon, S R, Brinton, L A, Berman, M L, Twiggs, L B, Barrett, R J, Wilbanks, G D, and Lurain, J R

Abstract

Background: Because intrauterine devices (IUD) invoke acute and chronic inflammatory responses in the endometrium, it is possible that prolonged insertion of an IUD could induce endometrial cancer.Methods: We examined the relation between use of an IUD and endometrial cancer risk using data from a multicentre case-control study involving 405 endometrial cancer cases and 297 population controls.Results: A total of 20 (4.9%) cases and 34 (11.4%) controls reported any use of an IUD. After adjustment for potential confounders, IUD use was not associated with an increased risk of endometrial cancer (RR = 0.56 for ever use; 95% CI: 0.3-1.0). Little reduction in risk was observed among women who last used an IUD within 10 years of the index date (RR = 0.84; 95% CI: 0.3-2.4) but risk was decreased among women who used an IUD in the more distant past (RR = 0.45; 95% CI: 0.2-1.0). Risk did not vary consistently with number of years of IUD use or with years since first use. Risk was not increased among women who used inert devices (RR = 0.46; 95% CI: 0.3-3.6) or those who used devices containing copper (RR = 1.08; 95% CI: 0.1-3.6).Conclusion: These data are reassuring in that they do not provide any evidence of an increased risk of endometrial cancer among women who have used IUD. [ABSTRACT FROM AUTHOR]

Published
1997
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50. Geographic variation in mortality from breast cancer among white women in the United States.

Author

Sturgeon SR, Schairer C, Gail M, McAdams M, Brinton LA, Hoover RN, Sturgeon, S R, Schairer, C, Gail, M, McAdams, M, Brinton, L A, and Hoover, R N

Abstract

Background: For several decades, mortality from breast cancer has been higher in the northeastern part of the United States than in other regions, particularly the South. Rates have also been somewhat higher in the Midwest and West than in the South, especially among older women. The reasons for these geographic variations are not well understood.Purpose: The objective of this study was to evaluate geographic differences in U.S. breast cancer mortality rates in 1987, after taking into account regional differences in the distribution of recognized breast cancer risk factors (e.g., late age at first live birth) and certain prognostic factors (e.g., mammography use).Methods: The 1987 breast cancer mortality rates for four regions of the country were obtained from the National Center for Health Statistics. Regional data on the distribution of breast cancer risk factors were obtained from 1987 National Health Interview Cancer Epidemiology Supplement interviews with 9778 white women aged 20-79 years. Regional data on the distribution of mammography use were obtained from 1987 National Health Interview Cancer Control Supplement interviews with 3795 white women aged 50-79 years.Results: Age-adjusted mortality ratios (MRs) among women 50 years and older were 1.15, 1.18, and 1.30 in the West, Midwest, and Northeast, respectively, compared with the South. Corresponding MRs among women 20-49 years old were 1.01, 1.08, and 1.07 in the West, Midwest, and Northeast, respectively, compared with the South. After adjustment for recognized risk factors and certain prognostic factors, MRs among older women were 1.13 (95% confidence interval [CI] = 1.04-1.23), 1.08 (95% CI = 1.01-1.16), and 1.13 (95% CI = 1.04-1.23) in the West, Midwest, and Northeast, respectively, compared with the South. Corresponding MRs among younger women were 0.94 (95% CI = 0.76-1.16), 1.05 (95% CI = 0.92-1.18), and 0.99 (95% CI = 0.86-1.14), respectively.Conclusion: Before adjustment for regional differences in recognized risk factors and prognostic factors, mortality excesses among younger women in the Northeast, Midwest, and West were less than 10% compared with the South. After adjustment, MRs were near unity for all regions. Among older women, the excess mortality was more substantial before adjustment for relevant factors, ranging from 15% in the West to 30% in the Northeast. Approximately 50% of the excesses in the Northeast and Midwest and 10% of the excess in the West could be explained on the basis of regional differences in the prevalence of recognized breast cancer risk factors and prognostic factors. After adjustment for these factors, the magnitude of excess in breast cancer mortality in the Northeast (13%) was comparable to that in the West (13%) but still slightly higher than that in the Midwest (8%). [ABSTRACT FROM AUTHOR]

Published
1995
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