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988 results on '"Ziegler, Regina"'

201. Factors associated with oxidative stress and cancer risk in the Breast and Prostate Cancer Cohort Consortium (BPC3)

Author

Blein, Sophie, Berndt, Sonja, Joshi, Amit D., Campa, Daniele, Ziegler, Regina G., Riboli, Elio, Cox, David G., Gaudet, Mia M., Stevens, Victoria L., Diver, W. Ryan, Gapstur, Susan M., Chanock, Stephen J., Hoover, Robert N., Yeager, Meredith, Albanes, Demetrius, Virtamo, Jarmo, Crawford, E. David, Isaacs, Claudine, Berg, Christine, Trichopoulos, Dimitrios, Panico, Salvatore, Peeters, Petra H., Johansson, Mattias, Khaw, Kay-Tee, Kraft, Peter, Hunter, David J., Lindström, Sara, Ma, Jing, Stampfer, Meir, Gaziano, J. Michael, Giovannucci, Edward, Willett, Walter H., Hankinson, Susan E., Lee, I-Min, Buring, Julie, Henderson, Brian, Le Marchand, Loïc, Kolonel, Laurence, and Haiman, Christopher J.

Subjects
Male, Oxidative Stress, Genotype, Humans, Prostatic Neoplasms, Breast Neoplasms, Female, Genetic Predisposition to Disease, Reactive Oxygen Species, Polymorphism, Single Nucleotide, Survival Analysis, Article
Abstract

Both endogenous factors (genomic variations) and exogenous factors (environmental exposures, lifestyle) impact the balance of reactive oxygen species (ROS). Variants of the ND3 (rs2853826; G10398A) gene of the mitochondrial genome, manganese superoxide dismutase (MnSOD; rs4880 Val16Ala) and glutathione peroxidase (GPX-1; rs1050450 Pro198Leu) are purported to have functional effects on regulation of ROS balance. In this study, we examined associations of breast and prostate cancer risk and survival with these variants, and interactions between rs4880 - rs1050450 and alcohol consumption - rs2853826. Nested case-control studies were conducted in the Breast and Prostate Cancer Cohort Consortium (BPC3), consisting of nine cohorts. The analyses included over 10726 post-menopausal breast and 7532 prostate cancer cases with matched controls. Logistic regression models were used to evaluate associations with risk, and proportional hazard models were used for survival outcomes. We did not observe significant interactions between polymorphisms in MnSOD and GPX-1, or between mitochondrial polymorphisms and alcohol intake and risk of either breast (p-interaction of 0.34 and 0.98 respectively) or prostate cancer (p-interaction of 0.49 and 0.50 respectively). We observed a weak inverse association between prostate cancer risk and GPX-1 Leu198Leu carriers (OR 0.87, 95% CI 0.79 – 0.97, p = 0.01). Overall survival among women with breast cancer was inversely associated with G10398 carriers who consumed alcohol (HR 0.66 95% CI 0.49 – 0.88). Given the high power in our study, it is unlikely that interactions tested have more than moderate effects on breast or prostate cancer risk. Observed associations need both further epidemiological and biological confirmation.

Published
2014

202. A comprehensive examination of breast cancer risk loci in African American women

Author

Bandera, Elisa V., John, Esther M., Palmer, Julie R., Olshan, Andrew F., Chanock, Stephen J., Ziegler, Regina G., Press, Michael F., Millikan, Robert C., Chen, Gary K., Hu, Jennifer J., Nyante, Sarah, Conti, David V., Ingles, Sue A., Zheng, Wei, Ambrosone, Christine B., Kolonel, Laurence N., Easton, Douglas, Stram, Alex, Park, Karen, Henderson, Brian E., Le Marchand, Loic, Rhie, Suhn Kyong, Ogundiran, Temidayo, Stram, Daniel O., Deming, Sandra L., Rodriguez-Gil, Jorge L., Bernstein, Leslie, Huo, Dezheng, Adebamowo, Clement A., Rand, Kristin A., Feng, Ye, and Olopade, Olufunmilayo I.

Abstract

Genome-wide association studies have identified 73 breast cancer risk variants mainly in European populations. Given considerable differences in linkage disequilibrium structure between populations of European and African ancestry, the known risk variants may not be informative for risk in African ancestry populations. In a previous fine-mapping investigation of 19 breast cancer loci, we were able to identify SNPs in four regions that better captured risk associations in African American women. In this study of breast cancer in African American women (3016 cases, 2745 controls), we tested an additional 54 novel breast cancer risk variants. Thirty-eight variants (70%) were found to have an association with breast cancer in the same direction as previously reported, with eight (15%) replicating at P < 0.05. Through fine-mapping, in three regions (1q32, 3p24, 10q25), we identified variants that better captured associations with overall breast cancer or estrogen receptor positive disease. We also observed suggestive associations with variants (at P < 5 × 10−6) in three separate regions (6q25, 14q13, 22q12) that may represent novel risk variants. Directional consistency of association observed for ∼65–70% of currently known genetic variants for breast cancer in women of African ancestry implies a shared functional common variant at most loci. To validate and enhance the spectrum of alleles that define associations at the known breast cancer risk loci, as well as genome-wide, will require even larger collaborative efforts in women of African ancestry.

Published
2014
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203. Additive interactions between susceptibility single-nucleotide polymorphisms identified in genome-wide association studies and breast cancer risk factors in the Breast and Prostate Cancer Cohort Consortium

Author

Joshi, Amit D., Lindström, Sara, Hüsing, Anika, Barrdahl, Myrto, VanderWeele, Tyler J., Campa, Daniele, Canzian, Federico, Gaudet, Mia M., Figueroa, Jonine D., Baglietto, Laura, Berg, Christine D., Buring, Julie E., Chanock, Stephen J., Chirlaque, María-Dolores, Diver, W. Ryan, Dossus, Laure, Giles, Graham G., Haiman, Christopher A., Hankinson, Susan E., Henderson, Brian E., Hoover, Robert N., Hunter, David J., Isaacs, Claudine, Kaaks, Rudolf, Kolonel, Laurence N., Krogh, Vittorio, Le Marchand, Loic, Lee, I-Min, Lund, Eiliv, McCarty, Catherine A., Overvad, Kim, Peeters, Petra H., Riboli, Elio, Schumacher, Fredrick, Severi, Gianluca, Stram, Daniel O., Sund, Malin, Thun, Michael J., Travis, Ruth C., Trichopoulos, Dimitrios, Willett, Walter C., Zhang, Shumin, Ziegler, Regina G., Kraft, Peter, and Marchand, Loic Le

Subjects
Male, Oncology, medicine.medical_specialty, Pathology, Epidemiology, Original Contributions, Additive interactions, Breast cancer, Genome-wide association studies, Single-nucleotide polymorphisms, Breast Neoplasms, Single-nucleotide polymorphism, Genome-wide association study, Polymorphism, Single Nucleotide, Risk Assessment, White People, Body Mass Index, Cohort Studies, Prostate cancer, Risk Factors, Internal medicine, Biomarkers, Tumor, Odds Ratio, Humans, Medicine, Genetic Predisposition to Disease, Alleles, business.industry, Australia, Absolute risk reduction, Case-control study, Prostatic Neoplasms, Odds ratio, Middle Aged, medicine.disease, United States, DNA-Binding Proteins, Europe, Case-Control Studies, Female, Rad51 Recombinase, business, Risk assessment, Genome-Wide Association Study
Abstract

Additive interactions can have public health and etiological implications but are infrequently reported. We assessed departures from additivity on the absolute risk scale between 9 established breast cancer risk factors and 23 susceptibility single-nucleotide polymorphisms (SNPs) identified from genome-wide association studies among 10,146 non-Hispanic white breast cancer cases and 12,760 controls within the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium. We estimated the relative excess risk due to interaction and its 95% confidence interval for each pairwise combination of SNPs and nongenetic risk factors using age- and cohort-adjusted logistic regression models. After correction for multiple comparisons, we identified a statistically significant relative excess risk due to interaction (uncorrected P = 4.51 × 10(-5)) between a SNP in the DNA repair protein RAD51 homolog 2 gene (RAD51L1; rs10483813) and body mass index (weight (kg)/height (m)(2)). We also compared additive and multiplicative polygenic risk prediction models using per-allele odds ratio estimates from previous studies for breast-cancer susceptibility SNPs and observed that the multiplicative model had a substantially better goodness of fit than the additive model.

Published
2014

204. Breast Cancer Risk From Modifiable and Nonmodifiable Risk Factors Among White Women in the United States

Author

Maas, Paige, primary, Barrdahl, Myrto, additional, Joshi, Amit D., additional, Auer, Paul L., additional, Gaudet, Mia M., additional, Milne, Roger L., additional, Schumacher, Fredrick R., additional, Anderson, William F., additional, Check, David, additional, Chattopadhyay, Subham, additional, Baglietto, Laura, additional, Berg, Christine D., additional, Chanock, Stephen J., additional, Cox, David G., additional, Figueroa, Jonine D., additional, Gail, Mitchell H., additional, Graubard, Barry I., additional, Haiman, Christopher A., additional, Hankinson, Susan E., additional, Hoover, Robert N., additional, Isaacs, Claudine, additional, Kolonel, Laurence N., additional, Le Marchand, Loic, additional, Lee, I-Min, additional, Lindström, Sara, additional, Overvad, Kim, additional, Romieu, Isabelle, additional, Sanchez, Maria-Jose, additional, Southey, Melissa C., additional, Stram, Daniel O., additional, Tumino, Rosario, additional, VanderWeele, Tyler J., additional, Willett, Walter C., additional, Zhang, Shumin, additional, Buring, Julie E., additional, Canzian, Federico, additional, Gapstur, Susan M., additional, Henderson, Brian E., additional, Hunter, David J., additional, Giles, Graham G, additional, Prentice, Ross L., additional, Ziegler, Regina G., additional, Kraft, Peter, additional, Garcia-Closas, Montse, additional, and Chatterjee, Nilanjan, additional

Published
2016
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205. Admixture Mapping of African–American Women in the AMBER Consortium Identifies New Loci for Breast Cancer and Estrogen-Receptor Subtypes

Author

Ruiz-Narváez, Edward A., primary, Sucheston-Campbell, Lara, additional, Bensen, Jeannette T., additional, Yao, Song, additional, Haddad, Stephen, additional, Haiman, Christopher A., additional, Bandera, Elisa V., additional, John, Esther M., additional, Bernstein, Leslie, additional, Hu, Jennifer J., additional, Ziegler, Regina G., additional, Deming, Sandra L., additional, Olshan, Andrew F., additional, Ambrosone, Christine B., additional, Palmer, Julie R., additional, and Lunetta, Kathryn L., additional

Published
2016
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206. Genome-wide association studies in women of African ancestry identified 3q26.21 as a novel susceptibility locus for oestrogen receptor negative breast cancer

Author

Huo, Dezheng, primary, Feng, Ye, additional, Haddad, Stephen, additional, Zheng, Yonglan, additional, Yao, Song, additional, Han, Yoo-Jeong, additional, Ogundiran, Temidayo O., additional, Adebamowo, Clement, additional, Ojengbede, Oladosu, additional, Falusi, Adeyinka G., additional, Zheng, Wei, additional, Blot, William, additional, Cai, Qiuyin, additional, Signorello, Lisa, additional, John, Esther M., additional, Bernstein, Leslie, additional, Hu, Jennifer J., additional, Ziegler, Regina G., additional, Nyante, Sarah, additional, Bandera, Elisa V., additional, Ingles, Sue A., additional, Press, Michael F., additional, Deming, Sandra L., additional, Rodriguez-Gil, Jorge L., additional, Nathanson, Katherine L., additional, Domchek, Susan M., additional, Rebbeck, Timothy R., additional, Ruiz-Narváez, Edward A., additional, Sucheston-Campbell, Lara E., additional, Bensen, Jeannette T., additional, Simon, Michael S., additional, Hennis, Anselm, additional, Nemesure, Barbara, additional, Leske, M. Cristina, additional, Ambs, Stefan, additional, Chen, Lin S., additional, Qian, Frank, additional, Gamazon, Eric R., additional, Lunetta, Kathryn L., additional, Cox, Nancy J., additional, Chanock, Stephen J., additional, Kolonel, Laurence N., additional, Olshan, Andrew F., additional, Ambrosone, Christine B., additional, Olopade, Olufunmilayo I., additional, Palmer, Julie R., additional, and Haiman, Christopher A., additional

Published
2016
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207. Genetic variants in microRNA and microRNA biogenesis pathway genes and breast cancer risk among women of African ancestry

Author

Qian, Frank, primary, Feng, Ye, additional, Zheng, Yonglan, additional, Ogundiran, Temidayo O., additional, Ojengbede, Oladosu, additional, Zheng, Wei, additional, Blot, William, additional, Ambrosone, Christine B., additional, John, Esther M., additional, Bernstein, Leslie, additional, Hu, Jennifer J., additional, Ziegler, Regina G., additional, Nyante, Sarah, additional, Bandera, Elisa V., additional, Ingles, Sue A., additional, Press, Michael F., additional, Nathanson, Katherine L., additional, Hennis, Anselm, additional, Nemesure, Barbara, additional, Ambs, Stefan, additional, Kolonel, Laurence N., additional, Olopade, Olufunmilayo I., additional, Haiman, Christopher A., additional, and Huo, Dezheng, additional

Published
2016
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208. Female chromosome X mosaicism is age-related and preferentially affects the inactivated X chromosome

Author

Machiela, Mitchell J., primary, Zhou, Weiyin, additional, Karlins, Eric, additional, Sampson, Joshua N., additional, Freedman, Neal D., additional, Yang, Qi, additional, Hicks, Belynda, additional, Dagnall, Casey, additional, Hautman, Christopher, additional, Jacobs, Kevin B., additional, Abnet, Christian C., additional, Aldrich, Melinda C., additional, Amos, Christopher, additional, Amundadottir, Laufey T., additional, Arslan, Alan A., additional, Beane-Freeman, Laura E., additional, Berndt, Sonja I., additional, Black, Amanda, additional, Blot, William J., additional, Bock, Cathryn H., additional, Bracci, Paige M., additional, Brinton, Louise A., additional, Bueno-de-Mesquita, H Bas, additional, Burdett, Laurie, additional, Buring, Julie E., additional, Butler, Mary A., additional, Canzian, Federico, additional, Carreón, Tania, additional, Chaffee, Kari G., additional, Chang, I-Shou, additional, Chatterjee, Nilanjan, additional, Chen, Chu, additional, Chen, Constance, additional, Chen, Kexin, additional, Chung, Charles C., additional, Cook, Linda S., additional, Crous Bou, Marta, additional, Cullen, Michael, additional, Davis, Faith G., additional, De Vivo, Immaculata, additional, Ding, Ti, additional, Doherty, Jennifer, additional, Duell, Eric J., additional, Epstein, Caroline G., additional, Fan, Jin-Hu, additional, Figueroa, Jonine D., additional, Fraumeni, Joseph F., additional, Friedenreich, Christine M., additional, Fuchs, Charles S., additional, Gallinger, Steven, additional, Gao, Yu-Tang, additional, Gapstur, Susan M., additional, Garcia-Closas, Montserrat, additional, Gaudet, Mia M., additional, Gaziano, J. Michael, additional, Giles, Graham G., additional, Gillanders, Elizabeth M., additional, Giovannucci, Edward L., additional, Goldin, Lynn, additional, Goldstein, Alisa M., additional, Haiman, Christopher A., additional, Hallmans, Goran, additional, Hankinson, Susan E., additional, Harris, Curtis C., additional, Henriksson, Roger, additional, Holly, Elizabeth A., additional, Hong, Yun-Chul, additional, Hoover, Robert N., additional, Hsiung, Chao A., additional, Hu, Nan, additional, Hu, Wei, additional, Hunter, David J., additional, Hutchinson, Amy, additional, Jenab, Mazda, additional, Johansen, Christoffer, additional, Khaw, Kay-Tee, additional, Kim, Hee Nam, additional, Kim, Yeul Hong, additional, Kim, Young Tae, additional, Klein, Alison P., additional, Klein, Robert, additional, Koh, Woon-Puay, additional, Kolonel, Laurence N., additional, Kooperberg, Charles, additional, Kraft, Peter, additional, Krogh, Vittorio, additional, Kurtz, Robert C., additional, LaCroix, Andrea, additional, Lan, Qing, additional, Landi, Maria Teresa, additional, Marchand, Loic Le, additional, Li, Donghui, additional, Liang, Xiaolin, additional, Liao, Linda M., additional, Lin, Dongxin, additional, Liu, Jianjun, additional, Lissowska, Jolanta, additional, Lu, Lingeng, additional, Magliocco, Anthony M., additional, Malats, Nuria, additional, Matsuo, Keitaro, additional, McNeill, Lorna H., additional, McWilliams, Robert R., additional, Melin, Beatrice S., additional, Mirabello, Lisa, additional, Moore, Lee, additional, Olson, Sara H., additional, Orlow, Irene, additional, Park, Jae Yong, additional, Patiño-Garcia, Ana, additional, Peplonska, Beata, additional, Peters, Ulrike, additional, Petersen, Gloria M., additional, Pooler, Loreall, additional, Prescott, Jennifer, additional, Prokunina-Olsson, Ludmila, additional, Purdue, Mark P., additional, Qiao, You-Lin, additional, Rajaraman, Preetha, additional, Real, Francisco X., additional, Riboli, Elio, additional, Risch, Harvey A., additional, Rodriguez-Santiago, Benjamin, additional, Ruder, Avima M., additional, Savage, Sharon A., additional, Schumacher, Fredrick, additional, Schwartz, Ann G., additional, Schwartz, Kendra L., additional, Seow, Adeline, additional, Wendy Setiawan, Veronica, additional, Severi, Gianluca, additional, Shen, Hongbing, additional, Sheng, Xin, additional, Shin, Min-Ho, additional, Shu, Xiao-Ou, additional, Silverman, Debra T., additional, Spitz, Margaret R., additional, Stevens, Victoria L., additional, Stolzenberg-Solomon, Rachael, additional, Stram, Daniel, additional, Tang, Ze-Zhong, additional, Taylor, Philip R., additional, Teras, Lauren R., additional, Tobias, Geoffrey S., additional, Van Den Berg, David, additional, Visvanathan, Kala, additional, Wacholder, Sholom, additional, Wang, Jiu-Cun, additional, Wang, Zhaoming, additional, Wentzensen, Nicolas, additional, Wheeler, William, additional, White, Emily, additional, Wiencke, John K., additional, Wolpin, Brian M., additional, Wong, Maria Pik, additional, Wu, Chen, additional, Wu, Tangchun, additional, Wu, Xifeng, additional, Wu, Yi-Long, additional, Wunder, Jay S., additional, Xia, Lucy, additional, Yang, Hannah P., additional, Yang, Pan-Chyr, additional, Yu, Kai, additional, Zanetti, Krista A., additional, Zeleniuch-Jacquotte, Anne, additional, Zheng, Wei, additional, Zhou, Baosen, additional, Ziegler, Regina G., additional, Perez-Jurado, Luis A., additional, Caporaso, Neil E., additional, Rothman, Nathaniel, additional, Tucker, Margaret, additional, Dean, Michael C., additional, Yeager, Meredith, additional, and Chanock, Stephen J., additional

Published
2016
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209. Endogenous Estrogens, Estrogen Metabolites, and Breast Cancer Risk in Postmenopausal Chinese Women

Author

Moore, Steven C., primary, Matthews, Charles E., additional, Ou Shu, Xiao, additional, Yu, Kai, additional, Gail, Mitchell H., additional, Xu, Xia, additional, Ji, Bu-Tian, additional, Chow, Wong-Ho, additional, Cai, Qiuyin, additional, Li, Honglan, additional, Yang, Gong, additional, Ruggieri, David, additional, Boyd-Morin, Jennifer, additional, Rothman, Nathaniel, additional, Hoover, Robert N., additional, Gao, Yu-Tang, additional, Zheng, Wei, additional, and Ziegler, Regina G., additional

Published
2016
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210. Associations between unprocessed red and processed meat, poultry, seafood and egg intake and the risk of prostate cancer: A pooled analysis of 15 prospective cohort studies

Author

Wu, Kana, primary, Spiegelman, Donna, additional, Hou, Tao, additional, Albanes, Demetrius, additional, Allen, Naomi E., additional, Berndt, Sonja I., additional, van den Brandt, Piet A., additional, Giles, Graham G., additional, Giovannucci, Edward, additional, Alexandra Goldbohm, R., additional, Goodman, Gary G., additional, Goodman, Phyllis J., additional, Håkansson, Niclas, additional, Inoue, Manami, additional, Key, Timothy J., additional, Kolonel, Laurence N., additional, Männistö, Satu, additional, McCullough, Marjorie L., additional, Neuhouser, Marian L., additional, Park, Yikyung, additional, Platz, Elizabeth A., additional, Schenk, Jeannette M., additional, Sinha, Rashmi, additional, Stampfer, Meir J., additional, Stevens, Victoria L., additional, Tsugane, Shoichiro, additional, Visvanathan, Kala, additional, Wilkens, Lynne R., additional, Wolk, Alicja, additional, Ziegler, Regina G., additional, and Smith-Warner, Stephanie A., additional

Published
2016
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211. Calibration and seasonal adjustment for matched case-control studies of vitamin D and cancer

Author

Gail, Mitchell H., primary, Wu, Jincao, additional, Wang, Molin, additional, Yaun, Shiaw-Shyuan, additional, Cook, Nancy R., additional, Eliassen, A. Heather, additional, McCullough, Marjorie L., additional, Yu, Kai, additional, Zeleniuch-Jacquotte, Anne, additional, Smith-Warner, Stephanie A., additional, Ziegler, Regina G., additional, and Carroll, Raymond J., additional

Published
2016
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214. Genetic risk variants associated with in situ breast cancer

Author

Campa, Daniele, Barrdahl, Myrto, Gaudet, Mia M., Black, Amanda, Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Haiman, Christopher, Hankinson, Susan, Hazra, Aditi, Henderson, Brian, Hoover, Robert N., Hunter, David J., Joshi, Amit D., Kraft, Peter, Le Marchand, Loic, Lindstrom, Sara, Willett, Walter, Travis, Ruth C., Amiano, Pilar, Siddiq, Afshan, Trichopoulos, Dimitrios, Sund, Malin, Tjonneland, Anne, Weiderpass, Elisabete, Peeters, Petra H., Panico, Salvatore, Dossus, Laure, Ziegler, Regina G., Canzian, Federico, Kaaks, Rudolf, Campa, Daniele, Barrdahl, Myrto, Gaudet, Mia M., Black, Amanda, Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Haiman, Christopher, Hankinson, Susan, Hazra, Aditi, Henderson, Brian, Hoover, Robert N., Hunter, David J., Joshi, Amit D., Kraft, Peter, Le Marchand, Loic, Lindstrom, Sara, Willett, Walter, Travis, Ruth C., Amiano, Pilar, Siddiq, Afshan, Trichopoulos, Dimitrios, Sund, Malin, Tjonneland, Anne, Weiderpass, Elisabete, Peeters, Petra H., Panico, Salvatore, Dossus, Laure, Ziegler, Regina G., Canzian, Federico, and Kaaks, Rudolf

Abstract

Introduction: Breast cancer in situ (BCIS) diagnoses, a precursor lesion for invasive breast cancer, comprise about 20 % of all breast cancers (BC) in countries with screening programs. Family history of BC is considered one of the strongest risk factors for BCIS. Methods: To evaluate the association of BC susceptibility loci with BCIS risk, we genotyped 39 single nucleotide polymorphisms (SNPs), associated with risk of invasive BC, in 1317 BCIS cases, 10,645 invasive BC cases, and 14,006 healthy controls in the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium (BPC3). Using unconditional logistic regression models adjusted for age and study, we estimated the association of SNPs with BCIS using two different comparison groups: healthy controls and invasive BC subjects to investigate whether BCIS and BC share a common genetic profile. Results: We found that five SNPs (CDKN2BAS-rs1011970, FGFR2-rs3750817, FGFR2-rs2981582, TNRC9-rs3803662, 5p12-rs10941679) were significantly associated with BCIS risk (P value adjusted for multiple comparisons <0.0016). Comparing invasive BC and BCIS, the largest difference was for CDKN2BAS-rs1011970, which showed a positive association with BCIS (OR = 1.24, 95 % CI: 1.11-1.38, P = 1.27 x 10(-4)) and no association with invasive BC (OR = 1.03, 95 % CI: 0.99-1.07, P = 0.06), with a P value for case-case comparison of 0.006. Subgroup analyses investigating associations with ductal carcinoma in situ (DCIS) found similar associations, albeit less significant (OR = 1.25, 95 % CI: 1.09-1.42, P = 1.07 x 10(-3)). Additional risk analyses showed significant associations with invasive disease at the 0.05 level for 28 of the alleles and the OR estimates were consistent with those reported by other studies. Conclusions: Our study adds to the knowledge that several of the known BC susceptibility loci are risk factors for both BCIS and invasive BC, with the possible exception of rs1011970, a putatively functional SNP situate

Published
2015
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215. Carotenoids, retinol, tocopherols, and prostate cancer risk : pooled analysis of 15 studies

Author

Key, Timothy J., Appleby, Paul N., Travis, Ruth C., Albanes, Demetrius, Alberg, Anthony J., Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Cook, Michael B., Donovan, Jenny L., Galan, Pilar, Gilbert, Rebecca, Giles, Graham G., Giovannucci, Edward, Goodman, Gary E., Goodman, Phyllis J., Gunter, Marc J., Hamdy, Freddie C., Heliovaara, Markku, Helzlsouer, Kathy J., Henderson, Brian E., Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N., Johansson, Mattias, Khaw, Kay-Tee, King, Irena B., Knekt, Paul, Kolonel, Laurence N., Le Marchand, Loic, Mannisto, Satu, Martin, Richard M., Meyer, Haakon E., Mondul, Alison M., Moy, Kristin A., Neal, David E., Neuhouser, Marian L., Palli, Domenico, Platz, Elizabeth A., Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M., Severi, Gianluca, Stampfer, Meir J., Tjonneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J., Ziegler, Regina G., Zhou, Cindy Ke, Allen, Naomi E., Key, Timothy J., Appleby, Paul N., Travis, Ruth C., Albanes, Demetrius, Alberg, Anthony J., Barricarte, Aurelio, Black, Amanda, Boeing, Heiner, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Cook, Michael B., Donovan, Jenny L., Galan, Pilar, Gilbert, Rebecca, Giles, Graham G., Giovannucci, Edward, Goodman, Gary E., Goodman, Phyllis J., Gunter, Marc J., Hamdy, Freddie C., Heliovaara, Markku, Helzlsouer, Kathy J., Henderson, Brian E., Hercberg, Serge, Hoffman-Bolton, Judy, Hoover, Robert N., Johansson, Mattias, Khaw, Kay-Tee, King, Irena B., Knekt, Paul, Kolonel, Laurence N., Le Marchand, Loic, Mannisto, Satu, Martin, Richard M., Meyer, Haakon E., Mondul, Alison M., Moy, Kristin A., Neal, David E., Neuhouser, Marian L., Palli, Domenico, Platz, Elizabeth A., Pouchieu, Camille, Rissanen, Harri, Schenk, Jeannette M., Severi, Gianluca, Stampfer, Meir J., Tjonneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J., Ziegler, Regina G., Zhou, Cindy Ke, and Allen, Naomi E.

Abstract

Background: Individual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease. Objective: The objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, alpha-tocopherol, and gamma-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors. Design: Principal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets. Results: Data were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For alpha-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). gamma-Tocopherol was not associated with risk. Conclusions: Overall prostate cancer risk was positively associated with retinol and inversely associated with alpha-tocopherol, and ris

Published
2015
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216. Association of breast cancer risk loci with breast cancer survival

Author

Barrdahl, Myrto, Canzian, Federico, Lindström, Sara, Shui, Irene, Black, Amanda, Hoover, Robert N, Ziegler, Regina G, Buring, Julie E, Chanock, Stephen J, Diver, W Ryan, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, Haiman, Christopher, Henderson, Brian E, Hankinson, Susan, Hunter, David J, Joshi, Amit D, Kraft, Peter, Lee, I-Min, Le Marchand, Loic, Milne, Roger L, Southey, Melissa C, Willett, Walter, Gunter, Marc, Panico, Salvatore, Sund, Malin, Weiderpass, Elisabete, Sánchez, María-José, Overvad, Kim, Dossus, Laure, Peeters, Petra H, Khaw, Kay-Tee, Trichopoulos, Dimitrios, Kaaks, Rudolf, Campa, Daniele, Barrdahl, Myrto, Canzian, Federico, Lindström, Sara, Shui, Irene, Black, Amanda, Hoover, Robert N, Ziegler, Regina G, Buring, Julie E, Chanock, Stephen J, Diver, W Ryan, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, Haiman, Christopher, Henderson, Brian E, Hankinson, Susan, Hunter, David J, Joshi, Amit D, Kraft, Peter, Lee, I-Min, Le Marchand, Loic, Milne, Roger L, Southey, Melissa C, Willett, Walter, Gunter, Marc, Panico, Salvatore, Sund, Malin, Weiderpass, Elisabete, Sánchez, María-José, Overvad, Kim, Dossus, Laure, Peeters, Petra H, Khaw, Kay-Tee, Trichopoulos, Dimitrios, Kaaks, Rudolf, and Campa, Daniele

Abstract

The survival of breast cancer patients is largely influenced by tumor characteristics, such as TNM stage, tumor grade and hormone receptor status. However, there is growing evidence that inherited genetic variation might affect the disease prognosis and response to treatment. Several lines of evidence suggest that alleles influencing breast cancer risk might also be associated with breast cancer survival. We examined the associations between 35 breast cancer susceptibility loci and the disease over-all survival (OS) in 10,255 breast cancer patients from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3) of which 1,379 died, including 754 of breast cancer. We also conducted a meta-analysis of almost 35,000 patients and 5,000 deaths, combining results from BPC3 and the Breast Cancer Association Consortium (BCAC) and performed in silico analyses of SNPs with significant associations. In BPC3, the C allele of LSP1-rs3817198 was significantly associated with improved OS (HRper-allele=0.70; 95% CI: 0.58-0.85; ptrend=2.84 x 10-4; HRheterozygotes=0.71; 95% CI: 0.55-0.92; HRhomozygotes=0.48; 95% CI: 0.31-0.76; p2DF=1.45 x 10-3). In silico, the C allele of LSP1-rs3817198 was predicted to increase expression of the tumor suppressor cyclin-dependent kinase inhibitor 1C (CDKN1C). In the meta-analysis, TNRC9-rs3803662 was significantly associated with increased death hazard (HRMETA =1.09; 95% CI: 1.04-1.15; ptrend=6.6 x 10-4; HRheterozygotes=0.96 95% CI: 0.90-1.03; HRhomozygotes=1.21; 95% CI: 1.09-1.35; p2DF=1.25 x 10-4). In conclusion, we show that there is little overlap between the breast cancer risk single nucleotide polymorphisms (SNPs) identified so far and the SNPs associated with breast cancer prognosis, with the possible exceptions of LSP1-rs3817198 and TNRC9-rs3803662. What's new? Genetic factors are known to influence the risk of breast cancer, but inherited genetic variation may also affect disease prognosis and response to treatment. In

Published
2015
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217. Vitamin D-Associated Genetic Variation and Risk of Breast Cancer in the Breast and Prostate Cancer Cohort Consortium (BPC3)

Author

Mondul, Alison M., Shui, Irene M., Yu, Kai, Weinstein, Stephanie J., Tsilidis, Konstantinos K., Joshi, Amit D., Agudo, Antonio, Berg, Christine D., Black, Amanda, Buring, Julie E., Chasman, Daniel I., Gaudet, Mia M., Haiman, Christopher, Hankinson, Susan E., Henderson, Brian E., Hoover, Robert N., Hunter, David J., Khaw, Kay-Tee, Kuehn, Tilman, Kvaskoff, Marina, Le Marchand, Loic, Lindstroem, Sara, McCullough, Marjorie L., Overvad, Kim, Peeters, Petra H., Riboli, Elio, Ridker, Paul M., Stram, Daniel O., Sund, Malin, Trichopoulos, Dimitrios, Tumino, Rosario, Weiderpass, Elisabete, Willett, Walter, Kraft, Peter, Ziegler, Regina G., Albanes, Demetrius, Mondul, Alison M., Shui, Irene M., Yu, Kai, Weinstein, Stephanie J., Tsilidis, Konstantinos K., Joshi, Amit D., Agudo, Antonio, Berg, Christine D., Black, Amanda, Buring, Julie E., Chasman, Daniel I., Gaudet, Mia M., Haiman, Christopher, Hankinson, Susan E., Henderson, Brian E., Hoover, Robert N., Hunter, David J., Khaw, Kay-Tee, Kuehn, Tilman, Kvaskoff, Marina, Le Marchand, Loic, Lindstroem, Sara, McCullough, Marjorie L., Overvad, Kim, Peeters, Petra H., Riboli, Elio, Ridker, Paul M., Stram, Daniel O., Sund, Malin, Trichopoulos, Dimitrios, Tumino, Rosario, Weiderpass, Elisabete, Willett, Walter, Kraft, Peter, Ziegler, Regina G., and Albanes, Demetrius

Abstract

Background: Two recent genome-wide association studies (GWAS) identified SNPs in or near four genes related to circulating 25-hydroxyvitamin D [25(OH) D] concentration. To examine the hypothesized inverse relationship between vitamin D status and breast cancer, we studied the associations between SNPs in these genes and breast cancer risk in a large pooled study of 9,456 cases and 10,816 controls from six cohorts. Methods: SNP markers localized to each of four genes (GC, CYP24A1, CYP2R1, and DHCR7) previously associated with 25 (OH) D were genotyped and examined both individually and as a 4-SNP polygenic score. Logistic regression was used to estimate the associations between the genetic variants and risk of breast cancer. Results: We found no association between any of the four SNPs or their polygenic score and breast cancer risk. Conclusions: Our findings do not support an association between vitamin D status, as reflected by 25(OH) D-related genotypes, and breast cancer risk. Impact: These findings may contribute to future meta-analyses and scientific review articles, and provide new data about the association between vitamin D-related genes and breast cancer.

Published
2015
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218. Characterization of Large Structural Genetic Mosaicism in Human Autosomes

Author

Machiela, Mitchell J., Zhou, Weiyin, Sampson, Joshua N., Dean, Michael C., Jacobs, Kevin B., Black, Amanda, Brinton, Louise A., Chang, I-Shou, Chen, Chu, Chen, Constance, Chen, Kexin, Cook, Linda S., Bou, Marta Crous, De Vivo, Immaculata, Doherty, Jennifer, Friedenreich, Christine M., Gaudet, Mia M., Haiman, Christopher A., Hankinson, Susan E., Hartge, Patricia, Henderson, Brian E., Hong, Yun-Chul, Hosgood, H. Dean, III, Hsiung, Chao A., Hu, Wei, Hunter, David J., Jessop, Lea, Kim, Hee Nam, Kim, Yeul Hong, Kim, Young Tae, Klein, Robert, Kraft, Peter, Lan, Qing, Lin, Dongxin, Liu, Jianjun, Le Marchand, Loic, Liang, Xiaolin, Lissowska, Jolanta, Lu, Lingeng, Magliocco, Anthony M., Matsuo, Keitaro, Olson, Sara H., Orlow, Irene, Park, Jae Yong, Pooler, Loreall, Prescott, Jennifer, Rastogi, Radhai, Risch, Harvey A., Schumacher, Fredrick, Seow, Adeline, Setiawan, Veronica Wendy, Shen, Hongbing, Sheng, Xin, Shin, Min-Ho, Shu, Xiao-Ou, VanDen Berg, David, Wang, Jiu-Cun, Wentzensen, Nicolas, Wong, Maria Pik, Wu, Chen, Wu, Tangchun, Wu, Yi-Long, Xia, Lucy, Yang, Hannah P., Yang, Pan-Chyr, Zheng, Wei, Zhou, Baosen, Abnet, Christian C., Albanes, Demetrius, Aldrich, Melinda C., Amos, Christopher, Amundadottir, Laufey T., Berndt, Sonja I., Blot, William J., Bock, Cathryn H., Bracci, Paige M., Burdett, Laurie, Buring, Julie E., Butler, Mary A., Carreon, Tania, Chatterjee, Nilanjan, Chung, Charles C., Cook, Michael B., Cullen, Michael, Davis, Faith G., Ding, Ti, Duell, Eric J., Epstein, Caroline G., Fan, Jin-Hu, Figueroa, Jonine D., Fraumeni, Joseph F., Jr., Freedman, Neal D., Fuchs, Charles S., Gao, Yu-Tang, Gapstur, Susan M., Patino-Garcia, Ana, Garcia-Closas, Montserrat, Gaziano, J. Michael, Giles, Graham G., Gillanders, Elizabeth M., Giovannucci, Edward L., Goldin, Lynn, Goldstein, Alisa M., Greene, Mark H., Hallmans, Göran, Harris, Curtis C., Henriksson, Roger, Holly, Elizabeth A., Hoover, Robert N., Hu, Nan, Hutchinson, Amy, Jenab, Mazda, Johansen, Christoffer, Khaw, Kay-Tee, Koh, Woon-Puay, Kolonel, Laurence N., Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C., LaCroix, Andrea, Landgren, Annelie, Landi, Maria Teresa, Li, Donghui, Liao, Linda M., Malats, Nuria, McGlynn, Katherine A., McNeill, Lorna H., McWilliams, Robert R., Melin, Beatrice S., Mirabello, Lisa, Peplonska, Beata, Peters, Ulrike, Petersen, Gloria M., Prokunina-Olsson, Ludmila, Purdue, Mark, Qiao, You-Lin, Rabe, Kari G., Rajaraman, Preetha, Real, Francisco X., Riboli, Elio, Rodriguez-Santiago, Benjamin, Rothman, Nathaniel, Ruder, Avima M., Savage, Sharon A., Schwartz, Ann G., Schwartz, Kendra L., Sesso, Howard D., Severi, Gianluca, Silverman, Debra T., Spitz, Margaret R., Stevens, Victoria L., Stolzenberg-Solomon, Rachael, Stram, Daniel, Tang, Ze-Zhong, Taylor, Philip R., Teras, Lauren R., Tobias, Geoffrey S., Viswanathan, Kala, Wacholder, Sholom, Wang, Zhaoming, Weinstein, Stephanie J., Wheeler, William, White, Emily, Wiencke, John K., Wolpin, Brian M., Wu, Xifeng, Wunder, Jay S., Yu, Kai, Zanetti, Krista A., Zeleniuch-Jacquotte, Anne, Ziegler, Regina G., De Andrade, Mariza, Barnes, Kathleen C., Beaty, Terri H., Bierut, Laura J., Desch, Karl C., Doheny, Kimberly F., Feenstra, Bjarke, Ginsburg, David, Heit, John A., Kang, Jae H., Laurie, Cecilia A., Li, Jun Z., Lowe, William L., Marazita, Mary L., Melbye, Mads, Mirel, Daniel B., Murray, Jeffrey C., Nelson, Sarah C., Pasquale, Louis R., Rice, Kenneth, Wiggs, Janey L., Wise, Anastasia, Tucker, Margaret, Perez-Jurado, Luis A., Laurie, Cathy C., Caporaso, Neil E., Yeager, Meredith, Chanock, Stephen J., Machiela, Mitchell J., Zhou, Weiyin, Sampson, Joshua N., Dean, Michael C., Jacobs, Kevin B., Black, Amanda, Brinton, Louise A., Chang, I-Shou, Chen, Chu, Chen, Constance, Chen, Kexin, Cook, Linda S., Bou, Marta Crous, De Vivo, Immaculata, Doherty, Jennifer, Friedenreich, Christine M., Gaudet, Mia M., Haiman, Christopher A., Hankinson, Susan E., Hartge, Patricia, Henderson, Brian E., Hong, Yun-Chul, Hosgood, H. Dean, III, Hsiung, Chao A., Hu, Wei, Hunter, David J., Jessop, Lea, Kim, Hee Nam, Kim, Yeul Hong, Kim, Young Tae, Klein, Robert, Kraft, Peter, Lan, Qing, Lin, Dongxin, Liu, Jianjun, Le Marchand, Loic, Liang, Xiaolin, Lissowska, Jolanta, Lu, Lingeng, Magliocco, Anthony M., Matsuo, Keitaro, Olson, Sara H., Orlow, Irene, Park, Jae Yong, Pooler, Loreall, Prescott, Jennifer, Rastogi, Radhai, Risch, Harvey A., Schumacher, Fredrick, Seow, Adeline, Setiawan, Veronica Wendy, Shen, Hongbing, Sheng, Xin, Shin, Min-Ho, Shu, Xiao-Ou, VanDen Berg, David, Wang, Jiu-Cun, Wentzensen, Nicolas, Wong, Maria Pik, Wu, Chen, Wu, Tangchun, Wu, Yi-Long, Xia, Lucy, Yang, Hannah P., Yang, Pan-Chyr, Zheng, Wei, Zhou, Baosen, Abnet, Christian C., Albanes, Demetrius, Aldrich, Melinda C., Amos, Christopher, Amundadottir, Laufey T., Berndt, Sonja I., Blot, William J., Bock, Cathryn H., Bracci, Paige M., Burdett, Laurie, Buring, Julie E., Butler, Mary A., Carreon, Tania, Chatterjee, Nilanjan, Chung, Charles C., Cook, Michael B., Cullen, Michael, Davis, Faith G., Ding, Ti, Duell, Eric J., Epstein, Caroline G., Fan, Jin-Hu, Figueroa, Jonine D., Fraumeni, Joseph F., Jr., Freedman, Neal D., Fuchs, Charles S., Gao, Yu-Tang, Gapstur, Susan M., Patino-Garcia, Ana, Garcia-Closas, Montserrat, Gaziano, J. Michael, Giles, Graham G., Gillanders, Elizabeth M., Giovannucci, Edward L., Goldin, Lynn, Goldstein, Alisa M., Greene, Mark H., Hallmans, Göran, Harris, Curtis C., Henriksson, Roger, Holly, Elizabeth A., Hoover, Robert N., Hu, Nan, Hutchinson, Amy, Jenab, Mazda, Johansen, Christoffer, Khaw, Kay-Tee, Koh, Woon-Puay, Kolonel, Laurence N., Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C., LaCroix, Andrea, Landgren, Annelie, Landi, Maria Teresa, Li, Donghui, Liao, Linda M., Malats, Nuria, McGlynn, Katherine A., McNeill, Lorna H., McWilliams, Robert R., Melin, Beatrice S., Mirabello, Lisa, Peplonska, Beata, Peters, Ulrike, Petersen, Gloria M., Prokunina-Olsson, Ludmila, Purdue, Mark, Qiao, You-Lin, Rabe, Kari G., Rajaraman, Preetha, Real, Francisco X., Riboli, Elio, Rodriguez-Santiago, Benjamin, Rothman, Nathaniel, Ruder, Avima M., Savage, Sharon A., Schwartz, Ann G., Schwartz, Kendra L., Sesso, Howard D., Severi, Gianluca, Silverman, Debra T., Spitz, Margaret R., Stevens, Victoria L., Stolzenberg-Solomon, Rachael, Stram, Daniel, Tang, Ze-Zhong, Taylor, Philip R., Teras, Lauren R., Tobias, Geoffrey S., Viswanathan, Kala, Wacholder, Sholom, Wang, Zhaoming, Weinstein, Stephanie J., Wheeler, William, White, Emily, Wiencke, John K., Wolpin, Brian M., Wu, Xifeng, Wunder, Jay S., Yu, Kai, Zanetti, Krista A., Zeleniuch-Jacquotte, Anne, Ziegler, Regina G., De Andrade, Mariza, Barnes, Kathleen C., Beaty, Terri H., Bierut, Laura J., Desch, Karl C., Doheny, Kimberly F., Feenstra, Bjarke, Ginsburg, David, Heit, John A., Kang, Jae H., Laurie, Cecilia A., Li, Jun Z., Lowe, William L., Marazita, Mary L., Melbye, Mads, Mirel, Daniel B., Murray, Jeffrey C., Nelson, Sarah C., Pasquale, Louis R., Rice, Kenneth, Wiggs, Janey L., Wise, Anastasia, Tucker, Margaret, Perez-Jurado, Luis A., Laurie, Cathy C., Caporaso, Neil E., Yeager, Meredith, and Chanock, Stephen J.

Abstract

Analyses of genome-wide association study (GWAS) data have revealed that detectable genetic mosaicism involving large (>2 Mb) structural autosomal alterations occurs in a fraction of individuals. We present results for a set of 24,849 genotyped individuals (total GWAS set II [TGSII]) in whom 341 large autosomal abnormalities were observed in 168 (0.68%) individuals. Merging data from the new TGSII set with data from two prior reports (the Gene-Environment Association Studies and the total GWAS set I) generated a large dataset of 127,179 individuals; we then conducted a meta-analysis to investigate the patterns of detectable autosomal mosaicism (n = 1,315 events in 925 [0.73%] individuals). Restricting to events >2 Mb in size, we observed an increase in event frequency as event size decreased. The combined results underscore that the rate of detectable mosaicism increases with age (p value = 5.5 x 3 10(-31)) and is higher in men (p value = 0.002) but lower in participants of African ancestry (p value = 0.003). In a subset of 47 individuals from whom serial samples were collected up to 6 years apart, complex changes were noted over time and showed an overall increase in the proportion of mosaic cells as age increased. Our large combined sample allowed for a unique ability to characterize detectable genetic mosaicism involving large structural events and strengthens the emerging evidence of non-random erosion of the genome in the aging population.

Published
2015
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219. Association of breast cancer risk loci with breast cancer survival

Author

Epi Kanker Team 1, JC onderzoeksprogramma Kanker, Cancer, Barrdahl, Myrto, Canzian, Federico, Lindström, Sara, Shui, Irene, Black, Amanda, Hoover, Robert N., Ziegler, Regina G., Buring, Julie E., Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Gaudet, Mia M., Giles, Graham G., Haiman, Christopher, Henderson, Brian E., Hankinson, Susan, Hunter, David J., Joshi, Amit D., Kraft, Peter, Lee, I. Min, Le Marchand, Loic, Milne, Roger L., Southey, Melissa C., Willett, Walter, Gunter, Marc, Panico, Salvatore, Sund, Malin, Weiderpass, Elisabete, Sánchez, María José, Overvad, Kim, Dossus, Laure, Peeters, Petra H., Khaw, Kay Tee, Trichopoulos, Dimitrios, Kaaks, Rudolf, Campa, Daniele, Epi Kanker Team 1, JC onderzoeksprogramma Kanker, Cancer, Barrdahl, Myrto, Canzian, Federico, Lindström, Sara, Shui, Irene, Black, Amanda, Hoover, Robert N., Ziegler, Regina G., Buring, Julie E., Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Gaudet, Mia M., Giles, Graham G., Haiman, Christopher, Henderson, Brian E., Hankinson, Susan, Hunter, David J., Joshi, Amit D., Kraft, Peter, Lee, I. Min, Le Marchand, Loic, Milne, Roger L., Southey, Melissa C., Willett, Walter, Gunter, Marc, Panico, Salvatore, Sund, Malin, Weiderpass, Elisabete, Sánchez, María José, Overvad, Kim, Dossus, Laure, Peeters, Petra H., Khaw, Kay Tee, Trichopoulos, Dimitrios, Kaaks, Rudolf, and Campa, Daniele

Published
2015

220. Genetic risk variants associated with in situ breast cancer

Author

Epi Kanker Team 1, JC onderzoeksprogramma Kanker, Cancer, Campa, Daniele, Barrdahl, Myrto, Gaudet, Mia M., Black, Amanda, Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Haiman, Christopher, Hankinson, Susan, Hazra, Aditi, Henderson, Brian, Hoover, Robert N., Hunter, David J., Joshi, Amit D., Kraft, Peter, Le Marchand, Loic, Lindstrom, Sara, Willett, Walter, Travis, Ruth C., Amiano, Pilar, Siddiq, Afshan, Trichopoulos, Dimitrios, Sund, Malin, Tjonneland, Anne, Weiderpass, Elisabete, Peeters, Petra H., Panico, Salvatore, Dossus, Laure, Ziegler, Regina G., Canzian, Federico, Kaaks, Rudolf, Epi Kanker Team 1, JC onderzoeksprogramma Kanker, Cancer, Campa, Daniele, Barrdahl, Myrto, Gaudet, Mia M., Black, Amanda, Chanock, Stephen J., Diver, W. Ryan, Gapstur, Susan M., Haiman, Christopher, Hankinson, Susan, Hazra, Aditi, Henderson, Brian, Hoover, Robert N., Hunter, David J., Joshi, Amit D., Kraft, Peter, Le Marchand, Loic, Lindstrom, Sara, Willett, Walter, Travis, Ruth C., Amiano, Pilar, Siddiq, Afshan, Trichopoulos, Dimitrios, Sund, Malin, Tjonneland, Anne, Weiderpass, Elisabete, Peeters, Petra H., Panico, Salvatore, Dossus, Laure, Ziegler, Regina G., Canzian, Federico, and Kaaks, Rudolf

Published
2015

221. Genetic Variation in the Vitamin D Pathway in Relation to Risk of Prostate Cancer:Results from Breast and Prostate Cancer Cohort Consortium (BPC3)

Author

Mondul, Alison M, Shui, Irene M, Yu, Kai, Travis, Ruth C, Stevens, Victoria L, Campa, Daniele, Schumacher, Frederick R, Ziegler, Regina G, Bueno-de-Mesquita, H Bas, Berndt, Sonja, Crawford, E David, Gapstur, Susan M, Gaziano, John Michael, Giovannucci, Edward, Haiman, Christopher A, Henderson, Brian E, Hunter, David J, Johansson, Mattias, Key, Timothy J, Le Marchand, Loic, Lindstrom, Sara, McCullough, Marjorie L, Navarro, Carmen, Overvad, Kim, Palli, Domenico, Purdue, Mark, Stampfer, Meir J, Weinstein, Stephanie J, Willett, Walter C, Yeager, Meredith, Chanock, Stephen J, Trichopoulos, Dimitrios, Kolonel, Laurence N, Kraft, Peter, and Albanes, Demetrius

Abstract

BACKGROUND: Studies suggest that vitamin D status may be associated with prostate cancer risk, although the direction and strength of this association differs between experimental and observational studies. Genome-wide association studies have identified genetic variants associated with 25-hydroxyvitamin D (25(OH)D) status. We examined SNPs in four genes shown to predict circulating levels of 25(OH)D in relation to prostate cancer risk. METHODS: SNP markers localized to each of four genes (GC, CYP24A1, CYP2R1, and DHCR7) previously associated with 25(OH)D were genotyped in 10,018 cases and 11,052 controls from the NCI Breast and Prostate Cancer Cohort Consortium. Logistic regression was used to estimate the individual and cumulative association between genetic variants and risk of overall and aggressive prostate cancer. RESULTS: We observed a decreased risk of aggressive prostate cancer among men with the allele in rs6013897 near CYP24A1 associated with lower serum 25(OH)D (per A allele, OR=0.86, 95%CI=0.80-0.93, p-trend=0.0002), but an increased risk for non-aggressive disease (per a allele: OR=1.10, 95%CI=1.04-1.17, p-trend=0.002). Examination of a polygenic score of the four SNPs revealed statistically significantly lower risk of aggressive prostate cancer among men with a greater number of low vitamin D alleles (OR for 6-8 vs. 0-1 alleles = 0.66, 95% CI = 0.44 - 0.98; p-trend=0.003). CONCLUSIONS: In this large, pooled analysis, genetic variants related to lower 25(OH)D were associated with a decreased risk of aggressive prostate cancer. Impact: Our genetic findings do not support a protective association between loci known to influence vitamin D levels and prostate cancer risk.

Published
2013

222. A genome-wide association study of breast cancer in women of African ancestry

Author

Ogundiran, Temidayo O., Chen, Fang, John, Esther M., Chanock, Stephen J., Cox, Nancy J., Palmer, Julie R., Zheng, Wei, Bernstein, Leslie, Hu, Jennifer J., Cai, Qiuyin, Nyante, Sarah, Ambrosone, Christine B., Bandera, Elisa V., Ruiz-Narvaez, Edward A., Long, Jirong, Ziegler, Regina G., Adebamowo, Clement, Rodriguez-Gil, Jorge L., Huo, Dezheng, Chen, Gary K., Blot, William, Stram, Daniel O., DeMichele, Angela, Li, Guoliang, Millikan, Robert C., Zheng, Yonglan, Signorello, Lisa, Rebbeck, Tim R., Olopade, Olufunmilayo I., Ingles, Sue A., Deming, Sandra L., and Press, Michael F.

Abstract

Genome-wide association studies (GWAS) in diverse populations are needed to reveal variants that are more common and/or limited to defined populations. We conducted a GWAS of breast cancer in women of African ancestry, with genotyping of > 1,000,000 SNPs in 3,153 African American cases and 2,831 controls, and replication testing of the top 66 associations in an additional 3,607 breast cancer cases and 11,330 controls of African ancestry. Two of the 66 SNPs replicated (p < 0.05) in stage 2, which reached statistical significance levels of 10−6 and 10−5 in the stage 1 and 2 combined analysis (rs4322600 at chromosome 14q31: OR = 1.18, p = 4.3×10−6; rs10510333 at chromosome 3p26: OR = 1.15, p = 1.5×10−5). These suggestive risk loci have not been identified in previous GWAS in other populations and will need to be examined in additional samples. Identification of novel risk variants for breast cancer in women of African ancestry will demand testing of a substantially larger set of markers from stage 1 in a larger replication sample.

Published
2013
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223. Genome-wide scan of 29,141 African Americans finds no evidence of selection since admixture

Author

Bhatia, Gaurav, Tandon, Arti, Aldrich, Melinda C., Ambrosone, Christine B., Amos, Christopher, Bandera, Elisa V., Berndt, Sonja I., Bernstein, Leslie, Blot, William J., Bock, Cathryn H., Caporaso, Neil, Casey, Graham, Deming, Sandra L., Diver, W. Ryan, Gapstur, Susan M., Gillanders, Elizabeth M., Harris, Curtis C., Henderson, Brian E., Ingles, Sue A., Isaacs, William, John, Esther M., Kittles, Rick A., Larkin, Emma, McNeill, Lorna H., Millikan, Robert C., Murphy, Adam, Neslund-Dudas, Christine, Nyante, Sarah, Press, Michael F., Rodriguez-Gil, Jorge L., Rybicki, Benjamin A., Schwartz, Ann G., Signorello, Lisa B., Spitz, Margaret, Strom, Sara S., Tucker, Margaret A., Wiencke, John K., Witte, John S., Wu, Xifeng, Yamamura, Yuko, Zanetti, Krista A., Zheng, Wei, Ziegler, Regina G., Chanock, Stephen J., Haiman, Christopher A., Reich, David, and Price, Alkes L.

Subjects
FOS: Biological sciences, Populations and Evolution (q-bio.PE), Quantitative Biology - Populations and Evolution
Abstract

We scanned through the genomes of 29,141 African Americans, searching for loci where the average proportion of African ancestry deviates significantly from the genome-wide average. We failed to find any genome-wide significant deviations, and conclude that any selection in African Americans since admixture is sufficiently weak that it falls below the threshold of our power to detect it using a large sample size. These results stand in contrast to the findings of a recent study of selection in African Americans. That study, which had 15 times fewer samples, reported six loci with significant deviations. We show that the discrepancy is likely due to insufficient correction for multiple hypothesis testing in the previous study. The same study reported 14 loci that showed greater population differentiation between African Americans and Nigerian Yoruba than would be expected in the absence of natural selection. Four such loci were previously shown to be genome-wide significant and likely to be affected by selection, but we show that most of the 10 additional loci are likely to be false positives. Additionally, the most parsimonious explanation for the loci that have significant evidence of unusual differentiation in frequency between Nigerians and Africans Americans is selection in Africa prior to their forced migration to the Americas.

Published
2013
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224. A comprehensive analysis of polymorphic variants in steroid hormone and insulin‐like growth factor‐1 metabolism and risk of <italic>in situ</italic> breast cancer: Results from the Breast and Prostate Cancer Cohort Consortium.

Author

Barrdahl, Myrto, Canzian, Federico, Gaudet, Mia M., Gapstur, Susan M., Trichopoulou, Antonia, Tsilidis, Kostas, van Gils, Carla H., Borgquist, Signe, Weiderpass, Elisabete, Khaw, Kay‐Tee, Giles, Graham G., Milne, Roger L., Le Marchand, Loic, Haiman, Christopher, Lindström, Sara, Kraft, Peter, Hunter, David J., Ziegler, Regina, Chanock, Stephen J., and Yang, Xiaohong R.

Abstract

We assessed the association between 1,414 single nucleotide polymorphisms (SNPs) in genes involved in synthesis and metabolism of steroid hormones and insulin‐like growth factor 1, and risk of breast cancer in situ (BCIS), with the aim of determining whether any of these were disease specific. This was carried out using 1,062 BCIS cases and 10,126 controls as well as 6,113 invasive breast cancer cases from the Breast and Prostate Cancer Cohort Consortium (BPC3). Three SNPs showed at least one nominally significant association in homozygous minor versus homozygous major models. ACVR2A‐rs2382112 (ORhom = 3.05, 95%CI = 1.72–5.44, Phom = 1.47 × 10−4), MAST2‐rs12124649 (ORhom = 1.73, 95% CI =1.18–2.54, Phom = 5.24 × 10−3), and INSR‐rs10500204 (ORhom = 1.96, 95% CI = 1.44–2.67, Phom=1.68 × 10−5) were associated with increased risk of BCIS; however, only the latter association was significant after correcting for multiple testing. Furthermore, INSR‐rs10500204 was more strongly associated with the risk of BCIS than invasive disease in case‐only analyses using the homozygous minor versus homozygous major model (ORhom = 1.78, 95% CI = 1.30–2.44, Phom = 3.23 × 10−4). The SNP INSR‐rs10500204 is located in an intron of the INSR gene and is likely to affect binding of the promyelocytic leukemia (PML) protein. The PML gene is known as a tumor suppressor and growth regulator in cancer. However, it is not clear on what pathway the A‐allele of rs10500204 could operate to influence the binding of the protein. Hence, functional studies are warranted to investigate this further. [ABSTRACT FROM AUTHOR]

Published
2018
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225. Carotenoid intakes and risk of breast cancer defined by estrogen receptor and progesterone receptor status: a pooled analysis of 18 prospective cohort studies123

Author

Zhang, Xuehong, Spiegelman, Donna, Baglietto, Laura, Bernstein, Leslie, Boggs, Deborah A, van den Brandt, Piet A, Buring, Julie E, Gapstur, Susan M, Giles, Graham G, Giovannucci, Edward, Goodman, Gary, Hankinson, Susan E, Helzlsouer, Kathy J, Horn-Ross, Pamela L, Inoue, Manami, Jung, Seungyoun, Khudyakov, Polyna, Larsson, Susanna C, Lof, Marie, McCullough, Marjorie L, Miller, Anthony B, Neuhouser, Marian L, Palmer, Julie R, Park, Yikyung, Robien, Kim, Rohan, Thomas E, Ross, Julie A, Schouten, Leo J, Shikany, James M, Tsugane, Shoichiro, Visvanathan, Kala, Weiderpass, Elisabete, Wolk, Alicja, Willett, Walter C, Zhang, Shumin M, Ziegler, Regina G, and Smith-Warner, Stephanie A

Subjects
Adult, Aged, 80 and over, Lutein, Breast Neoplasms, Middle Aged, Xanthophylls, beta Carotene, Carotenoids, Young Adult, Nutritional Epidemiology and Public Health, Receptors, Estrogen, Risk Factors, Zeaxanthins, Surveys and Questionnaires, Multivariate Analysis, Humans, Female, Prospective Studies, Receptors, Progesterone, Aged, Follow-Up Studies
Abstract

Epidemiologic studies examining associations between carotenoid intakes and risk of breast cancer by estrogen receptor (ER) and progesterone receptor (PR) status are limited.We investigated these associations in a pooled analysis of 18 cohort studies.Of 1,028,438 participants followed for a maximum follow-up of 26 y across studies, 33,380 incident invasive breast cancers were identified. Study-specific RRs and 95% CIs were estimated by using Cox proportional hazards regression and then pooled by using a random-effects model.α-Carotene, β-carotene, and lutein/zeaxanthin intakes were inversely associated with the risk of ER-negative (ER-) breast cancer (pooled multivariable RRs of the comparison between the highest and lowest quintiles): α-carotene (0.87; 95% CI: 0.78, 0.97), β-carotene (0.84; 95% CI: 0.77, 0.93), and lutein/zeaxanthin (0.87; 95% CI: 0.79, 0.95). These variables were not inversely associated with the risk of ER-positive (ER+) breast cancer (pooled multivariable RRs for the same comparison): α-carotene (1.04; 95% CI: 0.99, 1.09), β-carotene (1.04; 95% CI: 0.98, 1.10), and lutein/zeaxanthin (1.00; 95% CI: 0.93, 1.07). Although the pooled RRs for quintile 5 for β-cryptoxanthin were not significant, inverse trends were observed for ER- and ER+ breast cancer (P-trend ≤ 0.05). Nonsignificant associations were observed for lycopene intake. The associations were largely not appreciably modified by several breast cancer risk factors. Nonsignificant associations were observed for PR-positive and PR-negative breast cancer.Intakes of α-carotene, β-carotene, and lutein/zeaxanthin were inversely associated with risk of ER-, but not ER+, breast cancer. However, the results need to be interpreted with caution because it is unclear whether the observed association is real or due to other constituents in the same food sources.

Published
2012

226. Detectable clonal mosaicism and its relationship to aging and cancer

Author

Jacobs, Kevin B. Yeager, Meredith Zhou, Weiyin Wacholder, Sholom Wang, Zhaoming Rodriguez-Santiago, Benjamin and Hutchinson, Amy Deng, Xiang Liu, Chenwei Horner, Marie-Josephe Cullen, Michael Epstein, Caroline G. Burdett, Laurie Dean, Michael C. Chatterjee, Nilanjan Sampson, Joshua and Chung, Charles C. Kovaks, Joseph Gapstur, Susan M. and Stevens, Victoria L. Teras, Lauren T. Gaudet, Mia M. and Albanes, Demetrius Weinstein, Stephanie J. Virtamo, Jarmo and Taylor, Philip R. Freedman, Neal D. Abnet, Christian C. and Goldstein, Alisa M. Hu, Nan Yu, Kai Yuan, Jian-Min Liao, Linda Ding, Ti Qiao, You-Lin Gao, Yu-Tang Koh, Woon-Puay and Xiang, Yong-Bing Tang, Ze-Zhong Fan, Jin-Hu Aldrich, Melinda C. Amos, Christopher Blot, William J. Bock, Cathryn H. Gillanders, Elizabeth M. Harris, Curtis C. Haiman, Christopher A. Henderson, Brian E. Kolonel, Laurence N. Le Marchand, Loic McNeill, Lorna H. Rybicki, Benjamin A. and Schwartz, Ann G. Signorello, Lisa B. Spitz, Margaret R. and Wiencke, John K. Wrensch, Margaret Wu, Xifeng Zanetti, Krista A. Ziegler, Regina G. Figueroa, Jonine D. and Garcia-Closas, Montserrat Malats, Nuria Marenne, Gaelle and Prokunina-Olsson, Ludmila Baris, Dalsu Schwenn, Molly and Johnson, Alison Landi, Maria Teresa Goldin, Lynn Consonni, Dario Bertazzi, Pier Alberto Rotunno, Melissa Rajaraman, Preetha Andersson, Ulrika Freeman, Laura E. Beane Berg, Christine D. Buring, Julie E. Butler, Mary A. Carreon, Tania and Feychting, Maria Ahlbom, Anders Gaziano, J. Michael and Giles, Graham G. Hallmans, Goran Hankinson, Susan E. Hartge, Patricia Henriksson, Roger Inskip, Peter D. Johansen, Christoffer Landgren, Annelie McKean-Cowdin, Roberta and Michaud, Dominique S. Melin, Beatrice S. Peters, Ulrike and Ruder, Avima M. Sesso, Howard D. Severi, Gianluca Shu, Xiao-Ou Visvanathan, Kala White, Emily Wolk, Alicja and Zeleniuch-Jacquotte, Anne Zheng, Wei Silverman, Debra T. and Kogevinas, Manolis Gonzalez, Juan R. Villa, Olaya Li, Donghui Duell, Eric J. Risch, Harvey A. Olson, Sara H. and Kooperberg, Charles Wolpin, Brian M. Jiao, Li Hassan, Manal and Wheeler, William Arslan, Alan A. Bueno-de-Mesquita, H. Bas and Fuchs, Charles S. Gallinger, Steven Gross, Myron D. and Holly, Elizabeth A. Klein, Alison P. LaCroix, Andrea and Mandelson, Margaret T. Petersen, Gloria Boutron-Ruault, Marie-Christine Bracci, Paige M. Canzian, Federico Chang, Kenneth Cotterchio, Michelle Giovannucci, Edward L. Goggins, Michael Bolton, Judith A. Hoffman Jenab, Mazda Khaw, Kay-Tee and Krogh, Vittorio Kurtz, Robert C. McWilliams, Robert R. and Mendelsohn, Julie B. Rabe, Kari G. Riboli, Elio Tjonneland, Anne Tobias, Geoffrey S. Trichopoulos, Dimitrios Elena, Joanne W. Yu, Herbert Amundadottir, Laufey and Stolzenberg-Solomon, Rachael Z. Kraft, Peter Schumacher, Fredrick Stram, Daniel Savage, Sharon A. Mirabello, Lisa and Andrulis, Irene L. Wunder, Jay S. Patino Garcia, Ana and Sierrasesumaga, Luis Barkauskas, Donald A. Gorlick, Richard G. and Purdue, Mark Chow, Wong-Ho Moore, Lee E. Schwartz, Kendra L. Davis, Faith G. Hsing, Ann W. Berndt, Sonja I. and Black, Amanda Wentzensen, Nicolas Brinton, Louise A. and Lissowska, Jolanta Peplonska, Beata McGlynn, Katherine A. and Cook, Michael B. Graubard, Barry I. Kratz, Christian P. and Greene, Mark H. Erickson, Ralph L. Hunter, David J. Thomas, Gilles Hoover, Robert N. Real, Francisco X. Fraumeni, Jr., Joseph F. Caporaso, Neil E. Tucker, Margaret Rothman, Nathaniel Perez-Jurado, Luis A. Chanock, Stephen J.

Abstract

In an analysis of 31,717 cancer cases and 26,136 cancer-free controls from 13 genome-wide association studies, we observed large chromosomal abnormalities in a subset of clones in DNA obtained from blood or buccal samples. We observed mosaic abnormalities, either aneuploidy or copy-neutral loss of heterozygosity, of > 2 Mb in size in autosomes of 517 individuals (0.89%), with abnormal cell proportions of between 7% and 95%. In cancer-free individuals, frequency increased with age, from 0.23% under 50 years to 1.91% between 75 and 79 years (P = 4.8 x 10(-8)). Mosaic abnormalities were more frequent in individuals with solid tumors (0.97% versus 0.74% in cancer-free individuals; odds ratio (OR) = 1.25; P = 0.016), with stronger association with cases who had DNA collected before diagnosis or treatment (OR = 1.45; P = 0.0005). Detectable mosaicism was also more common in individuals for whom DNA was collected at least 1 year before diagnosis with leukemia compared to cancer-free individuals (OR = 35.4; P = 3.8 x 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases.

Published
2012

227. Enhanced Statistical Tests for GWAS in Admixed Populations: Assessment using African Americans from CARe and a Breast Cancer Consortium

Author

Nyante, Sarah J., Lange, Leslie A., Press, Michael F., Bandera, Elisa V., Cupples, L. Adrienne, Musani, Solomon K., Lettre, Guillaume, Zheng, Wei, Ingles, Sue A., Bernstein, Leslie, Chen, Gary K., Zaitlen, Noah, Siscovick, David S., Yang, Qiong, John, Esther M., Li, Mingyao, Chanock, Stephen J., Hu, Jennifer J., Akylbekova, Ermeg L., Zhu, Xiaofeng, Millikan, Robert C., Divers, Jasmin, Larkin, Emma, Kao, W. H. Linda, Pasaniuc, Bogdan, Ruczinski, Ingo, Mychaleckyj, Joe, Ambrosone, Christine B., Tandon, Arti, Fornage, Myriam, Ziegler, Regina G., and Papanicolaou, George J.

Abstract

While genome-wide association studies (GWAS) have primarily examined populations of European ancestry, more recent studies often involve additional populations, including admixed populations such as African Americans and Latinos. In admixed populations, linkage disequilibrium (LD) exists both at a fine scale in ancestral populations and at a coarse scale (admixture-LD) due to chromosomal segments of distinct ancestry. Disease association statistics in admixed populations have previously considered SNP association (LD mapping) or admixture association (mapping by admixture-LD), but not both. Here, we introduce a new statistical framework for combining SNP and admixture association in case-control studies, as well as methods for local ancestry-aware imputation. We illustrate the gain in statistical power achieved by these methods by analyzing data of 6,209 unrelated African Americans from the CARe project genotyped on the Affymetrix 6.0 chip, in conjunction with both simulated and real phenotypes, as well as by analyzing the FGFR2 locus using breast cancer GWAS data from 5,761 African-American women. We show that, at typed SNPs, our method yields an 8% increase in statistical power for finding disease risk loci compared to the power achieved by standard methods in case-control studies. At imputed SNPs, we observe an 11% increase in statistical power for mapping disease loci when our local ancestry-aware imputation framework and the new scoring statistic are jointly employed. Finally, we show that our method increases statistical power in regions harboring the causal SNP in the case when the causal SNP is untyped and cannot be imputed. Our methods and our publicly available software are broadly applicable to GWAS in admixed populations.

Published
2011
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228. A common variant at the TERT-CLPTM1L locus is associated with estrogen receptor-negative breast cancer

Author

Haiman, Christopher A. Chen, Gary K. Vachon, Celine M. and Canzian, Federico Dunning, Alison Millikan, Robert C. Wang, Xianshu Ademuyiwa, Foluso Ahmed, Shahana Ambrosone, Christine B. Baglietto, Laura Balleine, Rosemary Bandera, Elisa V. Beckmann, Matthias W. Berg, Christine D. Bernstein, Leslie Blomqvist, Carl Blot, William J. Brauch, Hiltrud and Buring, Julie E. Carey, Lisa A. Carpenter, Jane E. and Chang-Claude, Jenny Chanock, Stephen J. Chasman, Daniel I. and Clarke, Christine L. Cox, Angela Cross, Simon S. Deming, Sandra L. Diasio, Robert B. Dimopoulos, Athanasios M. and Driver, W. Ryan Duennebier, Thomas Durcan, Lorraine Eccles, Diana Edlund, Christopher K. Ekici, Arif B. Fasching, Peter A. Feigelson, Heather S. Flesch-Janys, Dieter Fostira, Florentia Foersti, Asta Fountzilas, George Gerty, Susan M. and Giles, Graham G. Godwin, Andrew K. Goodfellow, Paul and Graham, Nikki Greco, Dario Hamann, Ute Hankinson, Susan E. and Hartmann, Arndt Hein, Rebecca Heinz, Judith Holbrook, Andrea Hoover, Robert N. Hu, Jennifer J. Hunter, David J. and Ingles, Sue A. Irwanto, Astrid Ivanovich, Jennifer John, Esther M. Johnson, Nicola Jukkola-Vuorinen, Arja Kaaks, Rudolf Ko, Yon-Dschun Kolonel, Laurence N. Konstantopoulou, Irene Kosma, Veli-Matti Kulkarni, Swati Lambrechts, Diether and Lee, Adam M. Le Marchand, Loic Lesnick, Timothy Liu, Jianjun Lindstrom, Sara Mannermaa, Arto Margolin, Sara and Martin, Nicholas G. Miron, Penelope Montgomery, Grant W. and Nevanlinna, Heli Nickels, Stephan Nyante, Sarah Olswold, Curtis Palmer, Julie Pathak, Harsh Pectasides, Dimitrios and Perou, Charles M. Peto, Julian Pharoah, Paul D. P. Pooler, Loreall C. Press, Michael F. Pylkas, Katri Rebbeck, Timothy R. Rodriguez-Gil, Jorge L. Rosenberg, Lynn Ross, Eric and Ruediger, Thomas Silva, Isabel dos Santos Sawyer, Elinor and Schmidt, Marjanka K. Schulz-Wendtland, Ruediger Schumacher, Fredrick Severi, Gianluca Sheng, Xin Signorello, Lisa B. and Sinn, Hans-Peter Stevens, Kristen N. Southey, Melissa C. and Tapper, William J. Tomlinson, Ian Hogervorst, Frans B. L. and Wauters, Els Weaver, JoEllen Wildiers, Hans Winqvist, Robert and Van Den Berg, David Wan, Peggy Xia, Lucy Y. Yannoukakos, Drakoulis Zheng, Wei Ziegler, Regina G. Siddiq, Afshan and Slager, Susan L. Stram, Daniel O. Easton, Douglas Kraft, Peter Henderson, Brian E. Couch, Fergus J. Gene Environm Interaction Breast C

Abstract

Estrogen receptor (ER)-negative breast cancer shows a higher incidence in women of African ancestry compared to women of European ancestry. In search of common risk alleles for ER-negative breast cancer, we combined genome-wide association study (GWAS) data from women of African ancestry (1,004 ER-negative cases and 2,745 controls) and European ancestry (1,718 ER-negative cases and 3,670 controls), with replication testing conducted in an additional 2,292 ER-negative cases and 16,901 controls of European ancestry. We identified a common risk variant for ER-negative breast cancer at the TERT-CLPTM1L locus on chromosome 5p15 (rs10069690: per-allele odds ratio (OR) = 1.18 per allele, P = 1.0 x 10(-10)). The variant was also significantly associated with triple-negative (ER-negative, progesterone receptor (PR)-negative and human epidermal growth factor-2 (HER2)-negative) breast cancer (OR = 1.25, P = 1.1 x 10(-9)), particularly in younger women (

Published
2011

229. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies

Author

Key, Timothy J, primary, Appleby, Paul N, additional, Travis, Ruth C, additional, Albanes, Demetrius, additional, Alberg, Anthony J, additional, Barricarte, Aurelio, additional, Black, Amanda, additional, Boeing, Heiner, additional, Bueno-de-Mesquita, H Bas, additional, Chan, June M, additional, Chen, Chu, additional, Cook, Michael B, additional, Donovan, Jenny L, additional, Galan, Pilar, additional, Gilbert, Rebecca, additional, Giles, Graham G, additional, Giovannucci, Edward, additional, Goodman, Gary E, additional, Goodman, Phyllis J, additional, Gunter, Marc J, additional, Hamdy, Freddie C, additional, Heliövaara, Markku, additional, Helzlsouer, Kathy J, additional, Henderson, Brian E, additional, Hercberg, Serge, additional, Hoffman-Bolton, Judy, additional, Hoover, Robert N, additional, Johansson, Mattias, additional, Khaw, Kay-Tee, additional, King, Irena B, additional, Knekt, Paul, additional, Kolonel, Laurence N, additional, Le Marchand, Loic, additional, Männistö, Satu, additional, Martin, Richard M, additional, Meyer, Haakon E, additional, Mondul, Alison M, additional, Moy, Kristin A, additional, Neal, David E, additional, Neuhouser, Marian L, additional, Palli, Domenico, additional, Platz, Elizabeth A, additional, Pouchieu, Camille, additional, Rissanen, Harri, additional, Schenk, Jeannette M, additional, Severi, Gianluca, additional, Stampfer, Meir J, additional, Tjønneland, Anne, additional, Touvier, Mathilde, additional, Trichopoulou, Antonia, additional, Weinstein, Stephanie J, additional, Ziegler, Regina G, additional, Zhou, Cindy Ke, additional, and Allen, Naomi E, additional

Published
2015
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230. Eighteen Insulin-like Growth Factor (IGF) pathway genes, circulating levels of IGF-1 and its binding protein (IGFBP-3), and risk of prostate and breast cancer

Author

Gu, Fangyi, Schumacher, Fredrick R, Canzian, Federico, Allen, Naomi E, Albanes, Demetrius, Berg, Christine D, Berndt, Sonja I, Boeing, Heiner, Bueno-de-Mesquita, H Bas, Buring, Julie E, Chabbert-Buffet, Nathalie, Chanock, Stephen J, Clavel-Chapelon, Francoise, Dumeaux, Vanessa, J Michael Gaziano, J Michael Gaziano, Giovannucci, Edward, Haiman, Christopher A, Hankinson, Susan E, Hayes, Richard B, Henderson, Brian E, Hunter, David J, Hoover, Robert N, Johansson, Mattias, Key, Timothy J, Khaw, Kay-Tee, Kolonel, Laurence N, Lagiou, Pagona, Lee, I-Min, Lemarchand, Loïc, Lund, Eiliv, Ma, Jing, Onland-Moret, N Charlotte, Overvad, Kim, Rodriguez, Laudina, Sacerdote, Carlotta, Sanchez, Maria-Jose, Stampfer, Meir J, Stattin, Pär E, Stram, Daniel O, Thomas, Giles, Thun, Michael J, Tjonneland, Anne M, Trichopoulos, Dimitrios, Tumino, Rosario, Virtamo, Jarmo, Weinstein, Stephanie J, Willett, Walter C, Yeager, Meredith, Zhang, Shumin M, Kaaks, Rudolf, Riboli, Elio, Ziegler, Regina G, and Kraft, Peter L

Abstract

Udgivelsesdato: 2010-Sep-11 BACKGROUND: Circulating levels of insulin-like growth factor I (IGF-1) and its main binding protein, IGF binding protein 3 (IGFBP-3), have been associated with risk of several types of cancer. Heritable factors explain up to 60% of the variation in IGF-1 and IGFBP-3 in studies of adult twins. METHODS: We systematically examined common genetic variation in 18 genes in the IGF signaling pathway for associations with circulating levels of IGF-1 and IGFBP-3. A total of 302 single nucleotide polymorphisms (SNPs) were genotyped in over 5500 Caucasian men and 5500 Caucasian women from the Breast and Prostate Cancer Cohort Consortium (BPC3). RESULTS: After adjusting for multiple testing, SNPs in the IGF1 and SSTR5 genes were significantly associated with circulating IGF-1 (p

Published
2010

233. Alcohol consumption and breast cancer risk by estrogen receptor status: in a pooled analysis of 20 studies

Author

Jung, Seungyoun, primary, Wang, Molin, additional, Anderson, Kristin, additional, Baglietto, Laura, additional, Bergkvist, Leif, additional, Bernstein, Leslie, additional, van den Brandt, Piet A, additional, Brinton, Louise, additional, Buring, Julie E, additional, Heather Eliassen, A, additional, Falk, Roni, additional, Gapstur, Susan M, additional, Giles, Graham G, additional, Goodman, Gary, additional, Hoffman-Bolton, Judith, additional, Horn-Ross, Pamela L, additional, Inoue, Manami, additional, Kolonel, Laurence N, additional, Krogh, Vittorio, additional, Lof, Marie, additional, Maas, Paige, additional, Miller, Anthony B, additional, Neuhouser, Marian L, additional, Park, Yikyung, additional, Robien, Kim, additional, Rohan, Thomas E, additional, Scarmo, Stephanie, additional, Schouten, Leo J, additional, Sieri, Sabina, additional, Stevens, Victoria L, additional, Tsugane, Schoichiro, additional, Visvanathan, Kala, additional, Wilkens, Lynne R, additional, Wolk, Alicja, additional, Weiderpass, Elisabete, additional, Willett, Walter C, additional, Zeleniuch-Jacquotte, Anne, additional, Zhang, Shumin M, additional, Zhang, Xuehong, additional, Ziegler, Regina G, additional, and Smith-Warner, Stephanie A, additional

Published
2015
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234. Association of breast cancer risklociwith breast cancer survival

Author

Barrdahl, Myrto, primary, Canzian, Federico, additional, Lindström, Sara, additional, Shui, Irene, additional, Black, Amanda, additional, Hoover, Robert N., additional, Ziegler, Regina G., additional, Buring, Julie E., additional, Chanock, Stephen J., additional, Diver, W. Ryan, additional, Gapstur, Susan M., additional, Gaudet, Mia M., additional, Giles, Graham G., additional, Haiman, Christopher, additional, Henderson, Brian E., additional, Hankinson, Susan, additional, Hunter, David J., additional, Joshi, Amit D., additional, Kraft, Peter, additional, Lee, I-Min, additional, Le Marchand, Loic, additional, Milne, Roger L., additional, Southey, Melissa C., additional, Willett, Walter, additional, Gunter, Marc, additional, Panico, Salvatore, additional, Sund, Malin, additional, Weiderpass, Elisabete, additional, Sánchez, María-José, additional, Overvad, Kim, additional, Dossus, Laure, additional, Peeters, Petra H, additional, Khaw, Kay-Tee, additional, Trichopoulos, Dimitrios, additional, Kaaks, Rudolf, additional, and Campa, Daniele, additional

Published
2015
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235. ABO blood group alleles and prostate cancer risk: Results from the breast and prostate cancer cohort consortium (BPC3)

Author

Markt, Sarah C., primary, Shui, Irene M., additional, Unger, Robert H., additional, Urun, Yuksel, additional, Berg, Christine D., additional, Black, Amanda, additional, Brennan, Paul, additional, Bueno‐de‐Mesquita, H. Bas, additional, Gapstur, Susan M., additional, Giovannucci, Edward, additional, Haiman, Christopher, additional, Henderson, Brian, additional, Hoover, Robert N., additional, Hunter, David J., additional, Key, Timothy J., additional, Khaw, Kay‐Tee, additional, Canzian, Federico, additional, Larranga, Nerea, additional, Le Marchand, Loic, additional, Ma, Jing, additional, Naccarati, Alessio, additional, Siddiq, Afshan, additional, Stampfer, Meir J., additional, Stattin, Par, additional, Stevens, Victoria L., additional, Stram, Daniel O., additional, Tjønneland, Anne, additional, Travis, Ruth C., additional, Trichopoulos, Dimitrios, additional, Ziegler, Regina G., additional, Lindstrom, Sara, additional, Kraft, Peter, additional, Mucci, Lorelei A., additional, Choueiri, Toni K., additional, and Wilson, Kathryn M., additional

Published
2015
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239. Methodological Considerations in Estimation of Phenotype Heritability Using Genome-Wide SNP Data, Illustrated by an Analysis of the Heritability of Height in a Large Sample of African Ancestry Adults

Author

Chen, Fang, primary, He, Jing, additional, Zhang, Jianqi, additional, Chen, Gary K., additional, Thomas, Venetta, additional, Ambrosone, Christine B., additional, Bandera, Elisa V., additional, Berndt, Sonja I., additional, Bernstein, Leslie, additional, Blot, William J., additional, Cai, Qiuyin, additional, Carpten, John, additional, Casey, Graham, additional, Chanock, Stephen J., additional, Cheng, Iona, additional, Chu, Lisa, additional, Deming, Sandra L., additional, Driver, W. Ryan, additional, Goodman, Phyllis, additional, Hayes, Richard B., additional, Hennis, Anselm J. M., additional, Hsing, Ann W., additional, Hu, Jennifer J., additional, Ingles, Sue A., additional, John, Esther M., additional, Kittles, Rick A., additional, Kolb, Suzanne, additional, Leske, M. Cristina, additional, Millikan, Robert C., additional, Monroe, Kristine R., additional, Murphy, Adam, additional, Nemesure, Barbara, additional, Neslund-Dudas, Christine, additional, Nyante, Sarah, additional, Ostrander, Elaine A, additional, Press, Michael F., additional, Rodriguez-Gil, Jorge L., additional, Rybicki, Ben A., additional, Schumacher, Fredrick, additional, Stanford, Janet L., additional, Signorello, Lisa B., additional, Strom, Sara S., additional, Stevens, Victoria, additional, Van Den Berg, David, additional, Wang, Zhaoming, additional, Witte, John S., additional, Wu, Suh-Yuh, additional, Yamamura, Yuko, additional, Zheng, Wei, additional, Ziegler, Regina G., additional, Stram, Alexander H., additional, Kolonel, Laurence N., additional, Marchand, Loïc Le, additional, Henderson, Brian E., additional, Haiman, Christopher A., additional, and Stram, Daniel O., additional

Published
2015
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240. Genetic risk variants associated with in situ breast cancer

Author

Campa, Daniele, primary, Barrdahl, Myrto, additional, Gaudet, Mia M., additional, Black, Amanda, additional, Chanock, Stephen J., additional, Diver, W. Ryan, additional, Gapstur, Susan M., additional, Haiman, Christopher, additional, Hankinson, Susan, additional, Hazra, Aditi, additional, Henderson, Brian, additional, Hoover, Robert N., additional, Hunter, David J., additional, Joshi, Amit D., additional, Kraft, Peter, additional, Le Marchand, Loic, additional, Lindström, Sara, additional, Willett, Walter, additional, Travis, Ruth C., additional, Amiano, Pilar, additional, Siddiq, Afshan, additional, Trichopoulos, Dimitrios, additional, Sund, Malin, additional, Tjønneland, Anne, additional, Weiderpass, Elisabete, additional, Peeters, Petra H., additional, Panico, Salvatore, additional, Dossus, Laure, additional, Ziegler, Regina G., additional, Canzian, Federico, additional, and Kaaks, Rudolf, additional

Published
2015
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242. Characterization of Large Structural Genetic Mosaicism in Human Autosomes

Author

Machiela, Mitchell J., primary, Zhou, Weiyin, additional, Sampson, Joshua N., additional, Dean, Michael C., additional, Jacobs, Kevin B., additional, Black, Amanda, additional, Brinton, Louise A., additional, Chang, I-Shou, additional, Chen, Chu, additional, Chen, Constance, additional, Chen, Kexin, additional, Cook, Linda S., additional, Crous Bou, Marta, additional, De Vivo, Immaculata, additional, Doherty, Jennifer, additional, Friedenreich, Christine M., additional, Gaudet, Mia M., additional, Haiman, Christopher A., additional, Hankinson, Susan E., additional, Hartge, Patricia, additional, Henderson, Brian E., additional, Hong, Yun-Chul, additional, Hosgood, H. Dean, additional, Hsiung, Chao A., additional, Hu, Wei, additional, Hunter, David J., additional, Jessop, Lea, additional, Kim, Hee Nam, additional, Kim, Yeul Hong, additional, Kim, Young Tae, additional, Klein, Robert, additional, Kraft, Peter, additional, Lan, Qing, additional, Lin, Dongxin, additional, Liu, Jianjun, additional, Le Marchand, Loic, additional, Liang, Xiaolin, additional, Lissowska, Jolanta, additional, Lu, Lingeng, additional, Magliocco, Anthony M., additional, Matsuo, Keitaro, additional, Olson, Sara H., additional, Orlow, Irene, additional, Park, Jae Yong, additional, Pooler, Loreall, additional, Prescott, Jennifer, additional, Rastogi, Radhai, additional, Risch, Harvey A., additional, Schumacher, Fredrick, additional, Seow, Adeline, additional, Setiawan, Veronica Wendy, additional, Shen, Hongbing, additional, Sheng, Xin, additional, Shin, Min-Ho, additional, Shu, Xiao-Ou, additional, VanDen Berg, David, additional, Wang, Jiu-Cun, additional, Wentzensen, Nicolas, additional, Wong, Maria Pik, additional, Wu, Chen, additional, Wu, Tangchun, additional, Wu, Yi-Long, additional, Xia, Lucy, additional, Yang, Hannah P., additional, Yang, Pan-Chyr, additional, Zheng, Wei, additional, Zhou, Baosen, additional, Abnet, Christian C., additional, Albanes, Demetrius, additional, Aldrich, Melinda C., additional, Amos, Christopher, additional, Amundadottir, Laufey T., additional, Berndt, Sonja I., additional, Blot, William J., additional, Bock, Cathryn H., additional, Bracci, Paige M., additional, Burdett, Laurie, additional, Buring, Julie E., additional, Butler, Mary A., additional, Carreón, Tania, additional, Chatterjee, Nilanjan, additional, Chung, Charles C., additional, Cook, Michael B., additional, Cullen, Michael, additional, Davis, Faith G., additional, Ding, Ti, additional, Duell, Eric J., additional, Epstein, Caroline G., additional, Fan, Jin-Hu, additional, Figueroa, Jonine D., additional, Fraumeni, Joseph F., additional, Freedman, Neal D., additional, Fuchs, Charles S., additional, Gao, Yu-Tang, additional, Gapstur, Susan M., additional, Patiño-Garcia, Ana, additional, Garcia-Closas, Montserrat, additional, Gaziano, J. Michael, additional, Giles, Graham G., additional, Gillanders, Elizabeth M., additional, Giovannucci, Edward L., additional, Goldin, Lynn, additional, Goldstein, Alisa M., additional, Greene, Mark H., additional, Hallmans, Goran, additional, Harris, Curtis C., additional, Henriksson, Roger, additional, Holly, Elizabeth A., additional, Hoover, Robert N., additional, Hu, Nan, additional, Hutchinson, Amy, additional, Jenab, Mazda, additional, Johansen, Christoffer, additional, Khaw, Kay-Tee, additional, Koh, Woon-Puay, additional, Kolonel, Laurence N., additional, Kooperberg, Charles, additional, Krogh, Vittorio, additional, Kurtz, Robert C., additional, LaCroix, Andrea, additional, Landgren, Annelie, additional, Landi, Maria Teresa, additional, Li, Donghui, additional, Liao, Linda M., additional, Malats, Nuria, additional, McGlynn, Katherine A., additional, McNeill, Lorna H., additional, McWilliams, Robert R., additional, Melin, Beatrice S., additional, Mirabello, Lisa, additional, Peplonska, Beata, additional, Peters, Ulrike, additional, Petersen, Gloria M., additional, Prokunina-Olsson, Ludmila, additional, Purdue, Mark, additional, Qiao, You-Lin, additional, Rabe, Kari G., additional, Rajaraman, Preetha, additional, Real, Francisco X., additional, Riboli, Elio, additional, Rodríguez-Santiago, Benjamín, additional, Rothman, Nathaniel, additional, Ruder, Avima M., additional, Savage, Sharon A., additional, Schwartz, Ann G., additional, Schwartz, Kendra L., additional, Sesso, Howard D., additional, Severi, Gianluca, additional, Silverman, Debra T., additional, Spitz, Margaret R., additional, Stevens, Victoria L., additional, Stolzenberg-Solomon, Rachael, additional, Stram, Daniel, additional, Tang, Ze-Zhong, additional, Taylor, Philip R., additional, Teras, Lauren R., additional, Tobias, Geoffrey S., additional, Viswanathan, Kala, additional, Wacholder, Sholom, additional, Wang, Zhaoming, additional, Weinstein, Stephanie J., additional, Wheeler, William, additional, White, Emily, additional, Wiencke, John K., additional, Wolpin, Brian M., additional, Wu, Xifeng, additional, Wunder, Jay S., additional, Yu, Kai, additional, Zanetti, Krista A., additional, Zeleniuch-Jacquotte, Anne, additional, Ziegler, Regina G., additional, de Andrade, Mariza, additional, Barnes, Kathleen C., additional, Beaty, Terri H., additional, Bierut, Laura J., additional, Desch, Karl C., additional, Doheny, Kimberly F., additional, Feenstra, Bjarke, additional, Ginsburg, David, additional, Heit, John A., additional, Kang, Jae H., additional, Laurie, Cecilia A., additional, Li, Jun Z., additional, Lowe, William L., additional, Marazita, Mary L., additional, Melbye, Mads, additional, Mirel, Daniel B., additional, Murray, Jeffrey C., additional, Nelson, Sarah C., additional, Pasquale, Louis R., additional, Rice, Kenneth, additional, Wiggs, Janey L., additional, Wise, Anastasia, additional, Tucker, Margaret, additional, Pérez-Jurado, Luis A., additional, Laurie, Cathy C., additional, Caporaso, Neil E., additional, Yeager, Meredith, additional, and Chanock, Stephen J., additional

Published
2015
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243. Comparison of liquid chromatography-mass spectrometry, radioimmunoassay, and enzyme-linked immunosorbent assay methods for measurement of urinary estrogens

Author

Faupel-Badger, Jessica M., Fuhrman, Barbara J., Xu, Xia, Falk, Roni T., Keefer, Larry K., Veenstra, Timothy D., Hoover, Robert N., and Ziegler, Regina G.

Subjects
Adult, Postmenopause, Asian, Premenopause, Tandem Mass Spectrometry, Radioimmunoassay, Humans, Enzyme-Linked Immunosorbent Assay, Estrogens, Female, Middle Aged, Article, Chromatography, Liquid
Abstract

Absolute and relative concentrations of estrogens and estrogen metabolites are important for clinical decisions as well as for epidemiologic, experimental, and clinical research on hormonal carcinogenesis. RIA and ELISA are routinely used for measuring estrogen metabolites in blood and urine due to efficiency and low cost. Here, we compare absolute and ranked concentrations of estrone, estradiol, and estriol measured by indirect RIA and of 2-hydroxyestrone and 16alpha-hydroxyestrone measured by ELISA to the concentrations obtained using a novel liquid chromatography-tandem mass spectrometry (LC-MS/MS) method, which measures 15 estrogen metabolites concurrently. We used overnight urine samples collected from control women (362 premenopausal and 168 postmenopausal) participating in a population-based case-control study of breast cancer among Asian American women ages 20 to 55 years. When comparing RIA or ELISA levels to LC-MS/MS, absolute concentrations for the five estrogen metabolites ranged from 1.6 to 2.9 and 1.4 to 11.8 times higher in premenopausal and postmenopausal women, respectively (all P0.0001). However, LC-MS/MS measurements were highly correlated [Spearman r (r(s)) = 0.8-0.9] with RIA and ELISA measurements in premenopausal women and moderately correlated (r(s) = 0.4-0.8) in postmenopausal women. Measurements of the 2-hydroxyestrone:16alpha-hydroxyestrone ratio, a putative biomarker of breast cancer risk, were moderately correlated in premenopausal women (r(s) = 0.6-0.7) but only weakly correlated in postmenopausal women (r(s) = 0.2). LC-MS/MS had higher intraclass correlation coefficients (or =99.6%) and lower coefficients of variation (or =9.4%) than ELISA (or =97.2% andor =14.2%) and RIA (or =95.2% andor =17.8%). Comparison with the LC-MS/MS method suggests that the widely used RIA and ELISA estrogen metabolite measures may be problematic, especially at low estrogen metabolite levels characteristic of postmenopausal women.

Published
2010

244. Eighteen Insulin-like Growth Factor Pathway Genes, Circulating Levels of IGF-I and Its Binding Protein, and Risk of Prostate and Breast Cancer

Author

Gu, Fangyi Schumacher, Fredrick R. Canzian, Federico Allen, Naomi E. Albanes, Demetrius Berg, Christine D. Berndt, Sonja I. Boeing, Heiner Bueno-de-Mesquita, H. Bas Buring, Julie E. and Chabbert-Buffet, Nathalie Chanock, Stephen J. and Clavel-Chapelon, Francoise Dumeaux, Vanessa Gaziano, J. Michael and Giovannucci, Edward L. Haiman, Christopher A. Hankinson, Susan E. Hayes, Richard B. Henderson, Brian E. Hunter, David J. Hoover, Robert N. Johansson, Mattias Key, Timothy J. and Khaw, Kay-Tee Kolonel, Laurence N. Lagiou, Pagona Lee, I-Min and LeMarchand, Loic Lund, Eiliv Ma, Jing Onland-Moret, N. Charlotte Overvad, Kim Rodriguez, Laudina Sacerdote, Carlotta Sanchez, Maria-Jose Stampfer, Meir J. Stattin, Par and Stram, Daniel O. Thomas, Gilles Thun, Michael J. and Tjonneland, Anne Trichopoulos, Dimitrios Tumino, Rosario and Virtamo, Jarmo Weinstein, Stephanie J. Willett, Walter C. and Yeager, Meredith Zhang, Shumin M. Kaaks, Rudolf Riboli, Elio and Ziegler, Regina G. Kraft, Peter

Abstract

Background: Circulating levels of insulin-like growth factor I (IGF-I) and its main binding protein, IGF binding protein 3 (IGFBP-3), have been associated with risk of several types of cancer. Heritable factors explain up to 60% of the variation in IGF-I and IGFBP-3 in studies of adult twins. Methods: We systematically examined common genetic variation in 18 genes in the IGF signaling pathway for associations with circulating levels of IGF-I and IGFBP-3. A total of 302 single nucleotide polymorphisms (SNP) were genotyped in >5,500 Caucasian men and 5,500 Caucasian women from the Breast and Prostate Cancer Cohort Consortium. Results: After adjusting for multiple testing, SNPs in the IGF1 and SSTR5 genes were significantly associated with circulating IGF-I (P < 2.1 x 10(-4)); SNPs in the IGFBP3 and IGFALS genes were significantly associated with circulating IGFBP-3. Multi-SNP models explained R-2 = 0.62% of the variation in circulating IGF-I and 3.9% of the variation in circulating IGFBP-3. We saw no significant association between these multi-SNP predictors of circulating IGF-I or IGFBP-3 and risk of prostate or breast cancers. Conclusion: Common genetic variation in the IGF1 and SSTR5 genes seems to influence circulating IGF-I levels, and variation in IGFBP3 and IGFALS seems to influence circulating IGFBP-3. However, these variants explain only a small percentage of the variation in circulating IGF-I and IGFBP-3 in Caucasian men and women. Impact: Further studies are needed to explore contributions from other genetic factors such as rare variants in these genes and variation outside of these genes. Cancer Epidemiol Biomarkers Prev; 19(11); 2877-87. (C)2010 AACR.

Published
2010

245. Do we facilitate the scientific process and the development of dietary guidance when findings from single studies are publicized? An American Society for Nutritional Sciences Controversy Session Report

Author

Wellman, Nancy S, Scarbrough, F Edward, Ziegler, Regina G, and Lyle, Barbara

Subjects
Health attitudes -- Health aspects, Nutrition -- Media coverage, Health promotion -- Media coverage, Food/cooking/nutrition, Health
Abstract

This American Society for Nutritional Sciences Controversy Session presented at the 1997 Experimental Biology meeting considered whether publicity of findings from single studies facilitates or hampers the scientific process and the development of scientifically sound dietary guidance. In a 1995 survey, 78% of primary household shoppers believed it 'very likely' or 'somewhat likely' that in the next 5 y experts would have a completely different idea about which foods were healthy and which were not. This skepticism is fueled by the media's emphasis on reporting new and often controversial findings about food and nutrition. Media efforts are reinforced by the fact that some scientific journals regularly publicize newly published research findings. As a consequence, journalists frequently mediate scientific debate in a public forum--debate that previously was conducted among knowledgeable peers. Tight deadlines often make it difficult for reporters to thoroughly investigate findings publicized in press releases. Headlines can make results from single studies appear important, even when results are inconclusive. Finally, scientists and public policymakers have limited opportunity for making timely comments in response to an issue reported in the media. Nevertheless, the public has a right to be informed about health-related research findings to help them make decisions about their diets. The media are a valuable resource for educating the public and maintaining public interest in the importance of diet in overall health status. Nutrition scientists should be more involved in helping the media accurately convey diet and health messages. Am J Clin Nutr 1999;70:802-5. KEY WORDS Dietary guidance, publicity, science journalism, communicating research, media, nutrition

Published
1999

246. A genome-wide 'pleiotropy scan' does not identify new susceptibility loci for estrogen receptor negative breast cancer

Author

Campa, Daniele, Barrdahl, Myrto, Tsilidis, Konstantinos K, Severi, Gianluca, Diver, W Ryan, Siddiq, Afshan, Chanock, Stephen, Hoover, Robert N, Ziegler, Regina G, Berg, Christine D, Buys, Saundra S, Haiman, Christopher A, Henderson, Brian E, Schumacher, Fredrick R, Le Marchand, Loic, Flesch-Janys, Dieter, Lindstroem, Sara, Hunter, David J, Hankinson, Susan E, Willett, Walter C, Kraft, Peter, Cox, David G, Khaw, Kay-Tee, Tjonneland, Anne, Dossus, Laure, Trichopoulos, Dimitrios, Panico, Salvatore, van Gils, Carla H, Weiderpass, Elisabete, Barricarte, Aurelio, Sund, Malin, Gaudet, Mia M, Giles, Graham, Southey, Melissa, Baglietto, Laura, Chang-Claude, Jenny, Kaaks, Rudolf, Canzian, Federico, Campa, Daniele, Barrdahl, Myrto, Tsilidis, Konstantinos K, Severi, Gianluca, Diver, W Ryan, Siddiq, Afshan, Chanock, Stephen, Hoover, Robert N, Ziegler, Regina G, Berg, Christine D, Buys, Saundra S, Haiman, Christopher A, Henderson, Brian E, Schumacher, Fredrick R, Le Marchand, Loic, Flesch-Janys, Dieter, Lindstroem, Sara, Hunter, David J, Hankinson, Susan E, Willett, Walter C, Kraft, Peter, Cox, David G, Khaw, Kay-Tee, Tjonneland, Anne, Dossus, Laure, Trichopoulos, Dimitrios, Panico, Salvatore, van Gils, Carla H, Weiderpass, Elisabete, Barricarte, Aurelio, Sund, Malin, Gaudet, Mia M, Giles, Graham, Southey, Melissa, Baglietto, Laura, Chang-Claude, Jenny, Kaaks, Rudolf, and Canzian, Federico

Abstract

Approximately 15-30% of all breast cancer tumors are estrogen receptor negative (ER-). Compared with ER- positive (ER+) disease they have an earlier age at onset and worse prognosis. Despite the vast number of risk variants identified for numerous cancer types, only seven loci have been unambiguously identified for ER- negative breast cancer. With the aim of identifying new susceptibility SNPs for this disease we performed a pleiotropic genome-wide association study (GWAS). We selected 3079 SNPs associated with a human complex trait or disease at genome-wide significance level (P<5x10(-8)) to perform a secondary analysis of an ER- negative GWAS from the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium (BPC3), including 1998 cases and 2305 controls from prospective studies. We then tested the top ten associations (i.e. with the lowest P-values) using three additional populations with a total sample size of 3509 ER+ cases, 2543 ER- cases and 7031 healthy controls. None of the 3079 selected variants in the BPC3 ER- GWAS were significant at the adjusted threshold. 186 variants were associated with ER- breast cancer risk at a conventional threshold of P<0.05, with P-values ranging from 0.049 to 2.3 x 10(-4). None of the variants reached statistical significance in the replication phase. In conclusion, this study did not identify any novel susceptibility loci for ER-breast cancer using a "pleiotropic approach''.

Published
2014
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247. Post-G WAS gene-environment interplay in breast cancer : results from the Breast and Prostate Cancer Cohort Consortium and a meta-analysis on 79 000 women

Author

Barrdahl, Myrto, Canzian, Federico, Joshi, Amit D., Travis, Ruth C., Chang-Claude, Jenny, Auer, Paul L., Gapstur, Susan M., Gaudet, Mia, Diver, W. Ryan, Henderson, Brian E., Haiman, Christopher A., Schumacher, Fredrick R., Le Marchand, Loic, Berg, Christine D., Chanock, Stephen J., Hoover, Robert N., Rudolph, Anja, Ziegler, Regina G., Giles, Graham G., Baglietto, Laura, Severi, Gianluca, Hankinson, Susan E., Lindstroem, Sara, Willet, Walter, Hunter, David J., Buring, Julie E., Lee, I-Min, Zhang, Shumin, Dossus, Laure, Cox, David G., Khaw, Kay-Tee, Lund, Eiliv, Naccarati, Alessio, Peeters, Petra H., Ramon Quiros, J., Riboli, Elio, Sund, Malin, Trichopoulos, Dimitrios, Prentice, Ross L., Kraft, Peter, Kaaks, Rudolf, Campa, Daniele, Barrdahl, Myrto, Canzian, Federico, Joshi, Amit D., Travis, Ruth C., Chang-Claude, Jenny, Auer, Paul L., Gapstur, Susan M., Gaudet, Mia, Diver, W. Ryan, Henderson, Brian E., Haiman, Christopher A., Schumacher, Fredrick R., Le Marchand, Loic, Berg, Christine D., Chanock, Stephen J., Hoover, Robert N., Rudolph, Anja, Ziegler, Regina G., Giles, Graham G., Baglietto, Laura, Severi, Gianluca, Hankinson, Susan E., Lindstroem, Sara, Willet, Walter, Hunter, David J., Buring, Julie E., Lee, I-Min, Zhang, Shumin, Dossus, Laure, Cox, David G., Khaw, Kay-Tee, Lund, Eiliv, Naccarati, Alessio, Peeters, Petra H., Ramon Quiros, J., Riboli, Elio, Sund, Malin, Trichopoulos, Dimitrios, Prentice, Ross L., Kraft, Peter, Kaaks, Rudolf, and Campa, Daniele

Abstract

We studied the interplay between 39 breast cancer (BC) risk SNPs and established BC risk (body mass index, height, age at menarche, parity, age at menopause, smoking, alcohol and family history of BC) and prognostic factors (TNM stage, tumor grade, tumor size, age at diagnosis, estrogen receptor status and progesterone receptor status) as joint determinants of BC risk. We used a nested case-control design within the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium (BPC3), with 16 285 BC cases and 19 376 controls. We performed stratified analyses for both the risk and prognostic factors, testing for heterogeneity for the risk factors, and case-case comparisons for differential associations of polymorphisms by subgroups of the prognostic factors. We analyzed multiplicative interactions between the SNPs and the risk factors. Finally, we also performed a meta-analysis of the interaction ORs from BPC3 and the Breast Cancer Association Consortium. After correction for multiple testing, no significant interaction between the SNPs and the established risk factors in the BPC3 study was found. The meta-analysis showed a suggestive interaction between smoking status and SLC4A7-rs4973768 (P-interaction = 8.84 x 10(-4)) which, although not significant after considering multiple comparison, has a plausible biological explanation. In conclusion, in this study of up to almost 79 000 women we can conclusively exclude any novel major interactions between genome-wide association studies hits and the epidemiologic risk factors taken into consideration, but we propose a suggestive interaction between smoking status and SLC4A7-rs4973768 that if further replicated could help our understanding in the etiology of BC.

Published
2014
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248. Vitamin D–Associated Genetic Variation and Risk of Breast Cancer in the Breast and Prostate Cancer Cohort Consortium (BPC3)

Author

Mondul, Alison M., primary, Shui, Irene M., additional, Yu, Kai, additional, Weinstein, Stephanie J., additional, Tsilidis, Konstantinos K., additional, Joshi, Amit D., additional, Agudo, Antonio, additional, Berg, Christine D., additional, Black, Amanda, additional, Buring, Julie E., additional, Chasman, Daniel I., additional, Gaudet, Mia M., additional, Haiman, Christopher, additional, Hankinson, Susan E., additional, Henderson, Brian E., additional, Hoover, Robert N., additional, Hunter, David J., additional, Khaw, Kay-Tee, additional, Kühn, Tilman, additional, Kvaskoff, Marina, additional, Le Marchand, Loic, additional, Lindström, Sara, additional, McCullough, Marjorie L., additional, Overvad, Kim, additional, Peeters, Petra H., additional, Riboli, Elio, additional, Ridker, Paul M., additional, Stram, Daniel O., additional, Sund, Malin, additional, Trichopoulos, Dimitrios, additional, Tumino, Rosario, additional, Weiderpass, Elisabete, additional, Willett, Walter, additional, Kraft, Peter, additional, Ziegler, Regina G., additional, and Albanes, Demetrius, additional

Published
2014
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249. Assay Reproducibility and Interindividual Variation for 15 Serum Estrogens and Estrogen Metabolites Measured by Liquid Chromatography–Tandem Mass Spectrometry

Author

Fuhrman, Barbara J., primary, Xu, Xia, additional, Falk, Roni T., additional, Dallal, Cher M., additional, Veenstra, Timothy D., additional, Keefer, Larry K., additional, Graubard, Barry I., additional, Brinton, Louise A., additional, Ziegler, Regina G., additional, and Gierach, Gretchen L., additional

Published
2014
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250. Characterizing Genetic Susceptibility to Breast Cancer in Women of African Ancestry.

Author

Ye Feng, Suhn Kyong Rhie, Dezheng Huo, Ruiz-Narvaez, Edward A., Haddad, Stephen A., Ambrosone, Christine B., John, Esther M., Bernstein, Leslie, Wei Zheng, Hu, Jennifer J., Ziegler, Regina G., Nyante, Sarah, Bandera, Elisa V., Ingles, Sue A., Press, Michael F., Deming, Sandra L., Rodriguez-Gil, Jorge L., Yonglan Zheng, Song Yao, and Yoo-Jeong Han

Abstract

Background: Genome-wide association studies have identified approximately 100 common genetic variants associated with breast cancer risk, the majority of which were discovered in women of European ancestry. Because of different patterns of linkage disequilibrium, many of these genetic markers may not represent signals in populations of African ancestry. Methods: We tested 74 breast cancer risk variants and conducted fine-mapping of these susceptibility regions in 6,522 breast cancer cases and 7,643 controls of African ancestry from three genetic consortia (AABC, AMBER, and ROOT). Results: Fifty-four of the 74 variants (73%) were found to have ORs that were directionally consistent with those previously reported, of which 12 were nominally statistically significant (P < 0.05). Through fine-mapping, in six regions (3p24, 12p11, 14q13, 16q12/FTO, 16q23, 19p13), we observed seven markers that better represent the underlying risk variant for overall breast cancer or breast cancer subtypes, whereas in another two regions (11q13, 16q12/TOX3), we identified suggestive evidence of signals that are independent of the reported index variant. Overlapping chromatin features and regulatory elements suggest that many of the risk alleles lie in regions with biological functionality. Conclusions: Through fine-mapping of known susceptibility regions, we have revealed alleles that better characterize breast cancer risk in women of African ancestry. Impact: The risk alleles identified represent genetic markers for modeling and stratifying breast cancer risk in women of African ancestry. [ABSTRACT FROM AUTHOR]

Published
2017
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