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1. Characterizing prostate cancer risk through multi-ancestry genome-wide discovery of 187 novel risk variants

Author: Wang, Anqi, Shen, Jiayi, Rodriguez, Alex A., Saunders, Edward J., Chen, Fei, Janivara, Rohini, Darst, Burcu F., Sheng, Xin, Xu, Yili, Chou, Alisha J., Benlloch, Sara, Dadaev, Tokhir, Brook, Mark N., Plym, Anna, Sahimi, Ali, Hoffman, Thomas J., Takahashi, Atushi, Matsuda, Koichi, Momozawa, Yukihide, Fujita, Masashi, Laisk, Triin, Figuerêdo, Jéssica, Muir, Kenneth, Ito, Shuji, Liu, Xiaoxi, Uchio, Yuji, Kubo, Michiaki, Kamatani, Yoichiro, Lophatananon, Artitaya, Wan, Peggy, Andrews, Caroline, Lori, Adriana, Choudhury, Parichoy P., Schleutker, Johanna, Tammela, Teuvo L. J., Sipeky, Csilla, Auvinen, Anssi, Giles, Graham G., Southey, Melissa C., MacInnis, Robert J., Cybulski, Cezary, Wokolorczyk, Dominika, Lubinski, Jan, Rentsch, Christopher T., Cho, Kelly, Mcmahon, Benjamin H., Neal, David E., Donovan, Jenny L., Hamdy, Freddie C., Martin, Richard M., Nordestgaard, Borge G., Nielsen, Sune F., Weischer, Maren, Bojesen, Stig E., Røder, Andreas, Stroomberg, Hein V., Batra, Jyotsna, Chambers, Suzanne, Horvath, Lisa, Clements, Judith A., Tilly, Wayne, Risbridger, Gail P., Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordstrom, Tobias, Pashayan, Nora, Dunning, Alison M., Ghoussaini, Maya, Travis, Ruth C., Key, Tim J., Riboli, Elio, Park, Jong Y., Sellers, Thomas A., Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie, Cook, Michael B., Mucci, Lorelei A., Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David J., Penney, Kathryn L., Turman, Constance, Tangen, Catherine M., Goodman, Phyllis J., Thompson, Jr., Ian M., Hamilton, Robert J., Fleshner, Neil E., Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet L., Ostrander, Elaine A., Koutros, Stella, Beane Freeman, Laura E., Stampfer, Meir, Wolk, Alicja, Håkansson, Niclas, Andriole, Gerald L., Hoover, Robert N., Machiela, Mitchell J., Sørensen, Karina Dalsgaard, Borre, Michael, Blot, William J., Zheng, Wei, Yeboah, Edward D., Mensah, James E., Lu, Yong-Jie, Zhang, Hong-Wei, Feng, Ninghan, Mao, Xueying, Wu, Yudong, Zhao, Shan-Chao, Sun, Zan, Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., West, Catharine M. L., Barnett, Gill, Maier, Christiane, Schnoeller, Thomas, Luedeke, Manuel, Kibel, Adam S., Drake, Bettina F., Cussenot, Olivier, Cancel-Tassin, Geraldine, Menegaux, Florence, Truong, Thérèse, Koudou, Yves Akoli, John, Esther M., Grindedal, Eli Marie, Maehle, Lovise, Khaw, Kay-Tee, Ingles, Sue A., Stern, Mariana C., Vega, Ana, Gómez-Caamaño, Antonio, Fachal, Laura, Rosenstein, Barry S., Kerns, Sarah L., Ostrer, Harry, Teixeira, Manuel R., Paulo, Paula, Brandão, Andreia, Watya, Stephen, Lubwama, Alexander, Bensen, Jeannette T., Butler, Ebonee N., Mohler, James L., Taylor, Jack A., Kogevinas, Manolis, Dierssen-Sotos, Trinidad, Castaño-Vinyals, Gemma, Cannon-Albright, Lisa, Teerlink, Craig C., Huff, Chad D., Pilie, Patrick, Yu, Yao, Bohlender, Ryan J., Gu, Jian, Strom, Sara S., Multigner, Luc, Blanchet, Pascal, Brureau, Laurent, Kaneva, Radka, Slavov, Chavdar, Mitev, Vanio, Leach, Robin J., Brenner, Hermann, Chen, Xuechen, Holleczek, Bernd, Schöttker, Ben, Klein, Eric A., Hsing, Ann W., Kittles, Rick A., Murphy, Adam B., Logothetis, Christopher J., Kim, Jeri, Neuhausen, Susan L., Steele, Linda, Ding, Yuan Chun, Isaacs, William B., Nemesure, Barbara, Hennis, Anselm J. M., Carpten, John, Pandha, Hardev, Michael, Agnieszka, De Ruyck, Kim, De Meerleer, Gert, Ost, Piet, Xu, Jianfeng, Razack, Azad, Lim, Jasmine, Teo, Soo-Hwang, Newcomb, Lisa F., Lin, Daniel W., Fowke, Jay H., Neslund-Dudas, Christine M., Rybicki, Benjamin A., Gamulin, Marija, Lessel, Davor, Kulis, Tomislav, Usmani, Nawaid, Abraham, Aswin, Singhal, Sandeep, Parliament, Matthew, Claessens, Frank, Joniau, Steven, Van den Broeck, Thomas, Gago-Dominguez, Manuela, Castelao, Jose Esteban, Martinez, Maria Elena, Larkin, Samantha, Townsend, Paul A., Aukim-Hastie, Claire, Bush, William S., Aldrich, Melinda C., Crawford, Dana C., Srivastava, Shiv, Cullen, Jennifer, Petrovics, Gyorgy, Casey, Graham, Wang, Ying, Tettey, Yao, Lachance, Joseph, Tang, Wei, Biritwum, Richard B., Adjei, Andrew A., Tay, Evelyn, Truelove, Ann, Niwa, Shelley, Yamoah, Kosj, Govindasami, Koveela, Chokkalingam, Anand P., Keaton, Jacob M., Hellwege, Jacklyn N., Clark, Peter E., Jalloh, Mohamed, Gueye, Serigne M., Niang, Lamine, Ogunbiyi, Olufemi, Shittu, Olayiwola, Amodu, Olukemi, Adebiyi, Akindele O., Aisuodionoe-Shadrach, Oseremen I., Ajibola, Hafees O., Jamda, Mustapha A., Oluwole, Olabode P., Nwegbu, Maxwell, Adusei, Ben, Mante, Sunny, Darkwa-Abrahams, Afua, Diop, Halimatou, Gundell, Susan M., Roobol, Monique J., Jenster, Guido, van Schaik, Ron H. N., Hu, Jennifer J., Sanderson, Maureen, Kachuri, Linda, Varma, Rohit, McKean-Cowdin, Roberta, Torres, Mina, Preuss, Michael H., Loos, Ruth J. F., Zawistowski, Matthew, Zöllner, Sebastian, Lu, Zeyun, Van Den Eeden, Stephen K., Easton, Douglas F., Ambs, Stefan, Edwards, Todd L., Mägi, Reedik, Rebbeck, Timothy R., Fritsche, Lars, Chanock, Stephen J., Berndt, Sonja I., Wiklund, Fredrik, Nakagawa, Hidewaki, Witte, John S., Gaziano, J. Michael, Justice, Amy C., Mancuso, Nick, Terao, Chikashi, Eeles, Rosalind A., Kote-Jarai, Zsofia, Madduri, Ravi K., Conti, David V., and Haiman, Christopher A.
Published: 2023
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2. Circulating trans fatty acids are associated with prostate cancer in Ghanaian and American men

Author: Minas, Tsion Zewdu, Lord, Brittany D., Zhang, Amy L., Candia, Julián, Dorsey, Tiffany H., Baker, Francine S., Tang, Wei, Bailey-Whyte, Maeve, Smith, Cheryl J., Obadi, Obadi M., Ajao, Anuoluwapo, Jordan, Symone V., Tettey, Yao, Biritwum, Richard B., Adjei, Andrew A., Mensah, James E., Hoover, Robert N., Hsing, Ann W., Liu, Jia, Loffredo, Christopher A., Yates, Clayton, Cook, Michael B., and Ambs, Stefan
Published: 2023
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3. Common variants in breast cancer risk loci predispose to distinct tumor subtypes

Author: Ahearn, Thomas U, Zhang, Haoyu, Michailidou, Kyriaki, Milne, Roger L, Bolla, Manjeet K, Dennis, Joe, Dunning, Alison M, Lush, Michael, Wang, Qin, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Augustinsson, Annelie, Baten, Adinda, Becher, Heiko, Behrens, Sabine, Benitez, Javier, Bermisheva, Marina, Blomqvist, Carl, Bojesen, Stig E, Bonanni, Bernardo, Børresen-Dale, Anne-Lise, Brauch, Hiltrud, Brenner, Hermann, Brooks-Wilson, Angela, Brüning, Thomas, Burwinkel, Barbara, Buys, Saundra S, Canzian, Federico, Castelao, Jose E, Chang-Claude, Jenny, Chanock, Stephen J, Chenevix-Trench, Georgia, Clarke, Christine L, Collée, J Margriet, Cox, Angela, Cross, Simon S, Czene, Kamila, Daly, Mary B, Devilee, Peter, Dörk, Thilo, Dwek, Miriam, Eccles, Diana M, Evans, D Gareth, Fasching, Peter A, Figueroa, Jonine, Floris, Giuseppe, Gago-Dominguez, Manuela, Gapstur, Susan M, García-Sáenz, José A, Gaudet, Mia M, Giles, Graham G, Goldberg, Mark S, González-Neira, Anna, Alnæs, Grethe I Grenaker, Grip, Mervi, Guénel, Pascal, Haiman, Christopher A, Hall, Per, Hamann, Ute, Harkness, Elaine F, Heemskerk-Gerritsen, Bernadette AM, Holleczek, Bernd, Hollestelle, Antoinette, Hooning, Maartje J, Hoover, Robert N, Hopper, John L, Howell, Anthony, Jakimovska, Milena, Jakubowska, Anna, John, Esther M, Jones, Michael E, Jung, Audrey, Kaaks, Rudolf, Kauppila, Saila, Keeman, Renske, Khusnutdinova, Elza, Kitahara, Cari M, Ko, Yon-Dschun, Koutros, Stella, Kristensen, Vessela N, Krüger, Ute, Kubelka-Sabit, Katerina, Kurian, Allison W, Kyriacou, Kyriacos, Lambrechts, Diether, Lee, Derrick G, Lindblom, Annika, Linet, Martha, Lissowska, Jolanta, Llaneza, Ana, Lo, Wing-Yee, MacInnis, Robert J, Mannermaa, Arto, Manoochehri, Mehdi, Margolin, Sara, Martinez, Maria Elena, and McLean, Catriona
Subjects: Human Genome, Cancer, Genetics, Clinical Research, Breast Cancer, 2.1 Biological and endogenous factors, Aetiology, Biomarkers, Tumor, Breast Neoplasms, Female, Genome-Wide Association Study, Humans, Receptor, ErbB-2, Receptors, Estrogen, Receptors, Progesterone, Risk, Breast cancer, Etiologic heterogeneity, Genetic predisposition, Common breast cancer susceptibility variants, NBCS Collaborators, ABCTB Investigators, kConFab/AOCS Investigators, Receptor, erbB-2, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract: BackgroundGenome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear.MethodsAmong 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes.ResultsEighty-five of 173 variants were associated with at least one tumor feature (false discovery rate
Published: 2022

4. Combined Associations of a Polygenic Risk Score and Classical Risk Factors With Breast Cancer Risk.

Author: Kapoor, Pooja Middha, Mavaddat, Nasim, Choudhury, Parichoy Pal, Wilcox, Amber N, Lindström, Sara, Behrens, Sabine, Michailidou, Kyriaki, Dennis, Joe, Bolla, Manjeet K, Wang, Qin, Jung, Audrey, Abu-Ful, Zomoroda, Ahearn, Thomas, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Freeman, Laura E Beane, Becher, Heiko, Beckmann, Matthias W, Beeghly-Fadiel, Alicia, Benitez, Javier, Bernstein, Leslie, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brüning, Thomas, Cai, Qiuyin, Campa, Daniele, Canzian, Federico, Carracedo, Angel, Carter, Brian D, Castelao, Jose E, Chanock, Stephen J, Chatterjee, Nilanjan, Chenevix-Trench, Georgia, Clarke, Christine L, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Dai, James Y, Earp, H Shelton, Ekici, Arif B, Eliassen, A Heather, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Figueroa, Jonine, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gao, Chi, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, González-Neira, Anna, Guénel, Pascal, Haeberle, Lothar, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hamann, Ute, Hatse, Sigrid, Heyworth, Jane, Holleczek, Bernd, Hoover, Robert N, Hopper, John L, Howell, Anthony, Hunter, David J, ABCTB Investigators, kConFab/AOCS Investigators, John, Esther M, Jones, Michael E, Kaaks, Rudolf, Keeman, Renske, Kitahara, Cari M, Ko, Yon-Dschun, Koutros, Stella, Kurian, Allison W, Lambrechts, Diether, Le Marchand, Loic, Lee, Eunjung, Lejbkowicz, Flavio, Linet, Martha, Lissowska, Jolanta, Llaneza, Ana, MacInnis, Robert J, Martinez, Maria Elena, Maurer, Tabea, McLean, Catriona, Neuhausen, Susan L, Newman, William G, Norman, Aaron, O'Brien, Katie M, Olshan, Andrew F, Olson, Janet E, Olsson, Håkan, and Orr, Nick
Subjects: ABCTB Investigators, kConFab/AOCS Investigators, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract: We evaluated the joint associations between a new 313-variant PRS (PRS313) and questionnaire-based breast cancer risk factors for women of European ancestry, using 72 284 cases and 80 354 controls from the Breast Cancer Association Consortium. Interactions were evaluated using standard logistic regression and a newly developed case-only method for breast cancer risk overall and by estrogen receptor status. After accounting for multiple testing, we did not find evidence that per-standard deviation PRS313 odds ratio differed across strata defined by individual risk factors. Goodness-of-fit tests did not reject the assumption of a multiplicative model between PRS313 and each risk factor. Variation in projected absolute lifetime risk of breast cancer associated with classical risk factors was greater for women with higher genetic risk (PRS313 and family history) and, on average, 17.5% higher in the highest vs lowest deciles of genetic risk. These findings have implications for risk prevention for women at increased risk of breast cancer.
Published: 2021

5. In utero exposure to diethylstilbestrol and blood DNA methylation in adult women: Results from a meta-analysis of two cohort studies

Author: Bodelon, Clara, Gierach, Gretchen L., Hatch, Elizabeth E., Riseberg, Emily, Hutchinson, Amy, Yeager, Meredith, Sandler, Dale P., Taylor, Jack A., Hoover, Robert N., Xu, Zongli, Titus, Linda, Palmer, Julie R., and Troisi, Rebecca
Published: 2023
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6. Assessment of interactions between 205 breast cancer susceptibility loci and 13 established risk factors in relation to breast cancer risk, in the Breast Cancer Association Consortium

Author: Kapoor, Pooja Middha, Lindström, Sara, Behrens, Sabine, Wang, Xiaoliang, Michailidou, Kyriaki, Bolla, Manjeet K, Wang, Qin, Dennis, Joe, Dunning, Alison M, Pharoah, Paul DP, Schmidt, Marjanka K, Kraft, Peter, García-Closas, Montserrat, Easton, Douglas F, Milne, Roger L, Chang-Claude, Jenny, Ahearn, Thomas, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Augustinsson, Annelie, Freeman, Laura E Beane, Beckmann, Matthias W, Benitez, Javier, Bernstein, Leslie, Berrandou, Takiy, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brock, Ian W, Broeks, Annegien, Brooks-Wilson, Angela, Butterbach, Katja, Cai, Qiuyin, Campa, Daniele, Canzian, Federico, Carter, Brian D, Castelao, Jose E, Chanock, Stephen J, Chenevix-Trench, Georgia, Cheng, Ting-Yuan David, Clarke, Christine L, Cordina-Duverger, Emilie, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Dai, James Y, Dite, Gillian S, Earp, H Shelton, Eliassen, A Heather, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Figueroa, Jonine, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, González-Neira, Anna, Grundy, Anne, Guénel, Pascal, Haeberle, Lothar, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hamann, Ute, Hankinson, Susan E, Harkness, Elaine F, Harstad, Tricia, He, Wei, Heyworth, Jane, Hoover, Robert N, Hopper, John L, Humphreys, Keith, Hunter, David J, Marrón, Pablo Isidro, John, Esther M, Jones, Michael E, Jung, Audrey, Kaaks, Rudolf, Keeman, Renske, Kitahara, Cari M, Ko, Yon-Dschun, Koutros, Stella, Krüger, Ute, Lambrechts, Diether, Le Marchand, Loic, Lee, Eunjung, Lejbkowicz, Flavio, Linet, Martha, Lissowska, Jolanta, Llaneza, Ana, Lo, Wing-Yee, and Makalic, Enes
Subjects: Genetics, Estrogen, Clinical Research, Cancer, Breast Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Alleles, Breast Neoplasms, Case-Control Studies, Europe, Factor XIII, Female, Gene-Environment Interaction, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide, Receptors, Estrogen, Risk Factors, White People, Breast Cancer Association Consortium, Europeans, Gene-environment interaction, breast cancer, epidemiology, risk factors, single nucleotide polymorphism, Statistics, Public Health and Health Services, Epidemiology
Abstract: BackgroundPrevious gene-environment interaction studies of breast cancer risk have provided sparse evidence of interactions. Using the largest available dataset to date, we performed a comprehensive assessment of potential effect modification of 205 common susceptibility variants by 13 established breast cancer risk factors, including replication of previously reported interactions.MethodsAnalyses were performed using 28 176 cases and 32 209 controls genotyped with iCOGS array and 44 109 cases and 48 145 controls genotyped using OncoArray from the Breast Cancer Association Consortium (BCAC). Gene-environment interactions were assessed using unconditional logistic regression and likelihood ratio tests for breast cancer risk overall and by estrogen-receptor (ER) status. Bayesian false discovery probability was used to assess the noteworthiness of the meta-analysed array-specific interactions.ResultsNoteworthy evidence of interaction at ≤1% prior probability was observed for three single nucleotide polymorphism (SNP)-risk factor pairs. SNP rs4442975 was associated with a greater reduction of risk of ER-positive breast cancer [odds ratio (OR)int = 0.85 (0.78-0.93), Pint = 2.8 x 10-4] and overall breast cancer [ORint = 0.85 (0.78-0.92), Pint = 7.4 x 10-5) in current users of estrogen-progesterone therapy compared with non-users. This finding was supported by replication using OncoArray data of the previously reported interaction between rs13387042 (r2 = 0.93 with rs4442975) and current estrogen-progesterone therapy for overall disease (Pint = 0.004). The two other interactions suggested stronger associations between SNP rs6596100 and ER-negative breast cancer with increasing parity and younger age at first birth.ConclusionsOverall, our study does not suggest strong effect modification of common breast cancer susceptibility variants by established risk factors.
Published: 2020

7. Pubertal timing and breast density in young women: a prospective cohort study

Author: Houghton, Lauren C, Jung, Seungyoun, Troisi, Rebecca, LeBlanc, Erin S, Snetselaar, Linda G, Hylton, Nola M, Klifa, Catherine, Van Horn, Linda, Paris, Kenneth, Shepherd, John A, Hoover, Robert N, and Dorgan, Joanne F
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Cancer, Contraception/Reproduction, Clinical Research, Pediatric, Reproductive health and childbirth, Adolescent, Adult, Body Mass Index, Body Size, Breast, Breast Density, Breast Neoplasms, Child, Female, Humans, Magnetic Resonance Imaging, Menarche, Prospective Studies, Puberty, Risk Factors, Sexual Maturation, Time Factors, Breast cancer, Breast density, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract: BACKGROUND:Earlier age at onset of pubertal events and longer intervals between them (tempo) have been associated with increased breast cancer risk. It is unknown whether the timing and tempo of puberty are associated with adult breast density, which could mediate the increased risk. METHODS:From 1988 to 1997, girls participating in the Dietary Intervention Study in Children (DISC) were clinically assessed annually between ages 8 and 17 years for Tanner stages of breast development (thelarche) and pubic hair (pubarche), and onset of menses (menarche) was self-reported. In 2006-2008, 182 participants then aged 25-29 years had their percent dense breast volume (%DBV) measured by magnetic resonance imaging. Multivariable, linear mixed-effects regression models adjusted for reproductive factors, demographics, and body size were used to evaluate associations of age and tempo of puberty events with %DBV. RESULTS:The mean (standard deviation) and range of %DBV were 27.6 (20.5) and 0.2-86.1. Age at thelarche was negatively associated with %DBV (p trend = 0.04), while pubertal tempo between thelarche and menarche was positively associated with %DBV (p trend = 0.007). %DBV was 40% higher in women whose thelarche-to-menarche tempo was 2.9 years or longer (geometric mean (95%CI) = 21.8% (18.2-26.2%)) compared to women whose thelarche-to-menarche tempo was less than 1.6 years (geometric mean (95%CI) = 15.6% (13.9-17.5%)). CONCLUSIONS:Our results suggest that a slower pubertal tempo, i.e., greater number of months between thelarche and menarche, is associated with higher percent breast density in young women. Future research should examine whether breast density mediates the association between slower tempo and increased breast cancer risk.
Published: 2019

8. Targeted long-read sequencing of the Ewing sarcoma 6p25.1 susceptibility locus identifies germline-somatic interactions with EWSR1-FLI1 binding

Author: Lee, Olivia W., Rodrigues, Calvin, Lin, Shu-Hong, Luo, Wen, Jones, Kristine, Brown, Derek W., Zhou, Weiyin, Karlins, Eric, Khan, Sairah M., Baulande, Sylvain, Raynal, Virginie, Surdez, Didier, Reynaud, Stephanie, Rubio, Rebeca Alba, Zaidi, Sakina, Grossetête, Sandrine, Ballet, Stelly, Lapouble, Eve, Laurence, Valérie, Pierron, Gaelle, Gaspar, Nathalie, Corradini, Nadège, Marec-Bérard, Perrine, Rothman, Nathaniel, Dagnall, Casey L., Burdett, Laurie, Manning, Michelle, Wyatt, Kathleen, Yeager, Meredith, Chari, Raj, Leisenring, Wendy M., Kulozik, Andreas E., Kriebel, Jennifer, Meitinger, Thomas, Strauch, Konstantin, Kirchner, Thomas, Dirksen, Uta, Mirabello, Lisa, Tucker, Margaret A., Tirode, Franck, Armstrong, Gregory T., Bhatia, Smita, Robison, Leslie L., Yasui, Yutaka, Romero-Pérez, Laura, Hartmann, Wolfgang, Metzler, Markus, Diver, W. Ryan, Lori, Adriana, Freedman, Neal D., Hoover, Robert N., Morton, Lindsay M., Chanock, Stephen J., Grünewald, Thomas G.P., Delattre, Olivier, and Machiela, Mitchell J.
Published: 2023
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9. Associations of obesity and circulating insulin and glucose with breast cancer risk: a Mendelian randomization analysis.

Author: Shu, Xiang, Wu, Lang, Khankari, Nikhil K, Shu, Xiao-Ou, Wang, Thomas J, Michailidou, Kyriaki, Bolla, Manjeet K, Wang, Qin, Dennis, Joe, Milne, Roger L, Schmidt, Marjanka K, Pharoah, Paul DP, Andrulis, Irene L, Hunter, David J, Simard, Jacques, Easton, Douglas F, Zheng, Wei, Alicia, Beeghly-Fadiel J, Anton-Culver, Hoda, Antonenkova, Natalia N, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Barrdahl, Myrto, Baynes, Caroline, Beane Freeman, Laura E, Beckmann, Matthias W, Behrens, Sabine, Benitez, Javier, Bermisheva, Marina, Blomqvist, Carl, Bogdanova, Natalia V, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brinton, Louise, Broberg, Per, Brucker, Sara Y, Brüning, Thomas, Burwinkel, Barbara, Cai, Qiuyin, Caldés, Trinidad, Canzian, Federico, Carter, Brian D, Castelao, Jose E, Chang-Claude, Jenny, Chenevix-Trench, Georgia, David Cheng, Ting-Yuan, Clarke, Christine L, Conroy, Don M, Couch, Fergus J, Cox, David G, Cox, Angela, Cross, Simon S, Cunningham, Julie M, Czene, Kamila, Daly, Mary B, Doheny, Kimberly F, Dörk, Thilo, dos-Santos-Silva, Isabel, Dumont, Martine, Dunning, Alison M, Dwek, Miriam, Earp, H Shelton, Eccles, Diana M, Heather Eliassen, A, Engel, Christoph, Eriksson, Mikael, Gareth Evans, D, Fachal, Laura, Fasching, Peter A, Figueroa, Jonine, Fletcher, Olivia, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gapstur, Susan M, García-Closas, Montserrat, Gaudet, Mia M, Ghoussaini, Maya, Giles, Graham G, Goldberg, Mark S, Goldgar, David E, González-Neira, Anna, Guénel, Pascal, Hahnen, Eric, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hallberg, Emily, Hamann, Ute, Harrington, Patricia, He, Wei, Hein, Alexander, Hicks, Belynda, Hillemanns, Peter, Hogervorst, Frans B, Hollestelle, Antoinette, and Hoover, Robert N
Subjects: Clinical Research, Diabetes, Prevention, Nutrition, Obesity, Cancer, Aging, Breast Cancer, Genetics, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Adult, Aged, Blood Glucose, Body Mass Index, Breast Neoplasms, Diabetes Mellitus, Type 2, Female, Humans, Insulin, Mendelian Randomization Analysis, Middle Aged, Obesity, Abdominal, Waist-Hip Ratio, Breast cancer, insulin, glucose, obesity, genetics, Mendelian randomization analysis, Breast Cancer Association Consortium, Statistics, Public Health and Health Services, Epidemiology
Abstract: BackgroundIn addition to the established association between general obesity and breast cancer risk, central obesity and circulating fasting insulin and glucose have been linked to the development of this common malignancy. Findings from previous studies, however, have been inconsistent, and the nature of the associations is unclear.MethodsWe conducted Mendelian randomization analyses to evaluate the association of breast cancer risk, using genetic instruments, with fasting insulin, fasting glucose, 2-h glucose, body mass index (BMI) and BMI-adjusted waist-hip-ratio (WHRadj BMI). We first confirmed the association of these instruments with type 2 diabetes risk in a large diabetes genome-wide association study consortium. We then investigated their associations with breast cancer risk using individual-level data obtained from 98 842 cases and 83 464 controls of European descent in the Breast Cancer Association Consortium.ResultsAll sets of instruments were associated with risk of type 2 diabetes. Associations with breast cancer risk were found for genetically predicted fasting insulin [odds ratio (OR) = 1.71 per standard deviation (SD) increase, 95% confidence interval (CI) = 1.26-2.31, p = 5.09 × 10-4], 2-h glucose (OR = 1.80 per SD increase, 95% CI = 1.3 0-2.49, p = 4.02 × 10-4), BMI (OR = 0.70 per 5-unit increase, 95% CI = 0.65-0.76, p = 5.05 × 10-19) and WHRadj BMI (OR = 0.85, 95% CI = 0.79-0.91, p = 9.22 × 10-6). Stratified analyses showed that genetically predicted fasting insulin was more closely related to risk of estrogen-receptor [ER]-positive cancer, whereas the associations with instruments of 2-h glucose, BMI and WHRadj BMI were consistent regardless of age, menopausal status, estrogen receptor status and family history of breast cancer.ConclusionsWe confirmed the previously reported inverse association of genetically predicted BMI with breast cancer risk, and showed a positive association of genetically predicted fasting insulin and 2-h glucose and an inverse association of WHRadj BMI with breast cancer risk. Our study suggests that genetically determined obesity and glucose/insulin-related traits have an important role in the aetiology of breast cancer.
Published: 2019

10. Genome-wide association and transcriptome studies identify target genes and risk loci for breast cancer.

Author: Ferreira, Manuel A, Gamazon, Eric R, Al-Ejeh, Fares, Aittomäki, Kristiina, Andrulis, Irene L, Anton-Culver, Hoda, Arason, Adalgeir, Arndt, Volker, Aronson, Kristan J, Arun, Banu K, Asseryanis, Ella, Azzollini, Jacopo, Balmaña, Judith, Barnes, Daniel R, Barrowdale, Daniel, Beckmann, Matthias W, Behrens, Sabine, Benitez, Javier, Bermisheva, Marina, Białkowska, Katarzyna, Blomqvist, Carl, Bogdanova, Natalia V, Bojesen, Stig E, Bolla, Manjeet K, Borg, Ake, Brauch, Hiltrud, Brenner, Hermann, Broeks, Annegien, Burwinkel, Barbara, Caldés, Trinidad, Caligo, Maria A, Campa, Daniele, Campbell, Ian, Canzian, Federico, Carter, Jonathan, Carter, Brian D, Castelao, Jose E, Chang-Claude, Jenny, Chanock, Stephen J, Christiansen, Hans, Chung, Wendy K, Claes, Kathleen BM, Clarke, Christine L, EMBRACE Collaborators, GC-HBOC Study Collaborators, GEMO Study Collaborators, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Daly, Mary B, de la Hoya, Miguel, Dennis, Joe, Devilee, Peter, Diez, Orland, Dörk, Thilo, Dunning, Alison M, Dwek, Miriam, Eccles, Diana M, Ejlertsen, Bent, Ellberg, Carolina, Engel, Christoph, Eriksson, Mikael, Fasching, Peter A, Fletcher, Olivia, Flyger, Henrik, Friedman, Eitan, Frost, Debra, Gabrielson, Marike, Gago-Dominguez, Manuela, Ganz, Patricia A, Gapstur, Susan M, Garber, Judy, García-Closas, Montserrat, García-Sáenz, José A, Gaudet, Mia M, Giles, Graham G, Glendon, Gord, Godwin, Andrew K, Goldberg, Mark S, Goldgar, David E, González-Neira, Anna, Greene, Mark H, Gronwald, Jacek, Guénel, Pascal, Haiman, Christopher A, Hall, Per, Hamann, Ute, He, Wei, Heyworth, Jane, Hogervorst, Frans BL, Hollestelle, Antoinette, Hoover, Robert N, Hopper, John L, Hulick, Peter J, Humphreys, Keith, Imyanitov, Evgeny N, ABCTB Investigators, HEBON Investigators, and BCFR Investigators
Subjects: EMBRACE Collaborators, GC-HBOC Study Collaborators, GEMO Study Collaborators, ABCTB Investigators, HEBON Investigators, BCFR Investigators, Humans, Breast Neoplasms, Genetic Predisposition to Disease, Gene Expression Profiling, Quantitative Trait Loci, Female, Genome-Wide Association Study, Prevention, Cancer, Human Genome, Aging, Breast Cancer, Genetics, Biotechnology, 2.1 Biological and endogenous factors
Abstract: Genome-wide association studies (GWAS) have identified more than 170 breast cancer susceptibility loci. Here we hypothesize that some risk-associated variants might act in non-breast tissues, specifically adipose tissue and immune cells from blood and spleen. Using expression quantitative trait loci (eQTL) reported in these tissues, we identify 26 previously unreported, likely target genes of overall breast cancer risk variants, and 17 for estrogen receptor (ER)-negative breast cancer, several with a known immune function. We determine the directional effect of gene expression on disease risk measured based on single and multiple eQTL. In addition, using a gene-based test of association that considers eQTL from multiple tissues, we identify seven (and four) regions with variants associated with overall (and ER-negative) breast cancer risk, which were not reported in previous GWAS. Further investigation of the function of the implicated genes in breast and immune cells may provide insights into the etiology of breast cancer.
Published: 2019

11. Serum proteomics links suppression of tumor immunity to ancestry and lethal prostate cancer

Author: Minas, Tsion Zewdu, Candia, Julián, Dorsey, Tiffany H., Baker, Francine, Tang, Wei, Kiely, Maeve, Smith, Cheryl J., Zhang, Amy L., Jordan, Symone V., Obadi, Obadi M., Ajao, Anuoluwapo, Tettey, Yao, Biritwum, Richard B., Adjei, Andrew A., Mensah, James E., Hoover, Robert N., Jenkins, Frank J., Kittles, Rick, Hsing, Ann W., Wang, Xin W., Loffredo, Christopher A., Yates, Clayton, Cook, Michael B., and Ambs, Stefan
Published: 2022
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12. A transcriptome-wide association study of 229,000 women identifies new candidate susceptibility genes for breast cancer

Author: Wu, Lang, Shi, Wei, Long, Jirong, Guo, Xingyi, Michailidou, Kyriaki, Beesley, Jonathan, Bolla, Manjeet K, Shu, Xiao-Ou, Lu, Yingchang, Cai, Qiuyin, Al-Ejeh, Fares, Rozali, Esdy, Wang, Qin, Dennis, Joe, Li, Bingshan, Zeng, Chenjie, Feng, Helian, Gusev, Alexander, Barfield, Richard T, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Barrdahl, Myrto, Baynes, Caroline, Beckmann, Matthias W, Benitez, Javier, Bermisheva, Marina, Blomqvist, Carl, Bogdanova, Natalia V, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brinton, Louise, Broberg, Per, Brucker, Sara Y, Burwinkel, Barbara, Caldés, Trinidad, Canzian, Federico, Carter, Brian D, Castelao, J Esteban, Chang-Claude, Jenny, Chen, Xiaoqing, Cheng, Ting-Yuan David, Christiansen, Hans, Clarke, Christine L, NBCS Collaborators, Collée, Margriet, Cornelissen, Sten, Couch, Fergus J, Cox, David, Cox, Angela, Cross, Simon S, Cunningham, Julie M, Czene, Kamila, Daly, Mary B, Devilee, Peter, Doheny, Kimberly F, Dörk, Thilo, dos-Santos-Silva, Isabel, Dumont, Martine, Dwek, Miriam, Eccles, Diana M, Eilber, Ursula, Eliassen, A Heather, Engel, Christoph, Eriksson, Mikael, Fachal, Laura, Fasching, Peter A, Figueroa, Jonine, Flesch-Janys, Dieter, Fletcher, Olivia, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gapstur, Susan M, García-Closas, Montserrat, Gaudet, Mia M, Ghoussaini, Maya, Giles, Graham G, Goldberg, Mark S, Goldgar, David E, González-Neira, Anna, Guénel, Pascal, Hahnen, Eric, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hallberg, Emily, Hamann, Ute, Harrington, Patricia, Hein, Alexander, Hicks, Belynda, Hillemanns, Peter, Hollestelle, Antoinette, Hoover, Robert N, Hopper, John L, and Huang, Guanmengqian
Subjects: Biological Sciences, Genetics, Human Genome, Biotechnology, Prevention, Breast Cancer, Women's Health, Cancer Genomics, Cancer, 2.1 Biological and endogenous factors, Generic health relevance, Breast Neoplasms, Case-Control Studies, Female, Gene Expression, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Risk, Transcriptome, NBCS Collaborators, kConFab/AOCS Investigators, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract: The breast cancer risk variants identified in genome-wide association studies explain only a small fraction of the familial relative risk, and the genes responsible for these associations remain largely unknown. To identify novel risk loci and likely causal genes, we performed a transcriptome-wide association study evaluating associations of genetically predicted gene expression with breast cancer risk in 122,977 cases and 105,974 controls of European ancestry. We used data from the Genotype-Tissue Expression Project to establish genetic models to predict gene expression in breast tissue and evaluated model performance using data from The Cancer Genome Atlas. Of the 8,597 genes evaluated, significant associations were identified for 48 at a Bonferroni-corrected threshold of P
Published: 2018

13. Association of Estrogen Metabolism with Breast Cancer Risk in Different Cohorts of Postmenopausal Women

Author: Sampson, Joshua N, Falk, Roni T, Schairer, Catherine, Moore, Steven C, Fuhrman, Barbara J, Dallal, Cher M, Bauer, Douglas C, Dorgan, Joanne F, Shu, Xiao-Ou, Zheng, Wei, Brinton, Louise A, Gail, Mitchell H, Ziegler, Regina G, Xu, Xia, Hoover, Robert N, and Gierach, Gretchen L
Subjects: Cancer, Breast Cancer, Prevention, Estrogen, Clinical Research, Aging, Adult, Aged, Breast Neoplasms, Chromatography, Liquid, Cohort Studies, Estrogens, Female, Humans, Hydroxylation, Middle Aged, Postmenopause, Risk, Tandem Mass Spectrometry, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract: Endogenous estradiol and estrone are linked causally to increased risks of breast cancer. In this study, we evaluated multiple competing hypotheses for how metabolism of these parent estrogens may influence risk. Prediagnostic concentrations of estradiol, estrone, and 13 metabolites were measured in 1,298 postmenopausal cases of breast cancer and 1,524 matched controls in four separate patient cohorts. The median time between sample collection and diagnosis was 4.4 to 12.7 years across the cohorts. Estrogen analytes were measured in serum or urine by liquid chromatography-tandem mass spectrometry. Total estrogen levels (summing all 15 estrogens/estrogen metabolites) were associated strongly and positively with breast cancer risk. Normalizing total estrogen levels, we also found that a relative increase in levels of 2-hydroxylation pathway metabolites, or in the ratio of 2-hydroxylation:16-hydroxylation pathway metabolites, were associated inversely with breast cancer risk. These associations varied by total estrogen levels, with the largest risk reductions occurring in women in the highest tertile. With appropriate validation, these findings suggest opportunities for breast cancer prevention by modifying individual estrogen metabolism profiles through either lifestyle alterations or chemopreventive strategies. Cancer Res; 77(4); 918-25. ©2017 AACR.
Published: 2017

14. Circulating sex hormones in relation to anthropometric, sociodemographic and behavioural factors in an international dataset of 12,300 men

Author: Watts, Eleanor L, Appleby, Paul N, Albanes, Demetrius, Black, Amanda, Chan, June M, Chen, Chu, Cirillo, Piera M, Cohn, Barbara A, Cook, Michael B, Donovan, Jenny L, Ferrucci, Luigi, Garland, Cedric F, Giles, Graham G, Goodman, Phyllis J, Habel, Laurel A, Haiman, Christopher A, Holly, Jeff MP, Hoover, Robert N, Kaaks, Rudolf, Knekt, Paul, Kolonel, Laurence N, Kubo, Tatsuhiko, Le Marchand, Loïc, Luostarinen, Tapio, MacInnis, Robert J, Mäenpää, Hanna O, Männistö, Satu, Metter, E Jeffrey, Milne, Roger L, Nomura, Abraham MY, Oliver, Steven E, Parsons, J Kellogg, Peeters, Petra H, Platz, Elizabeth A, Riboli, Elio, Ricceri, Fulvio, Rinaldi, Sabina, Rissanen, Harri, Sawada, Norie, Schaefer, Catherine A, Schenk, Jeannette M, Stanczyk, Frank Z, Stampfer, Meir, Stattin, Pär, Stenman, Ulf-Håkan, Tjønneland, Anne, Trichopoulou, Antonia, Thompson, Ian M, Tsugane, Shoichiro, Vatten, Lars, Whittemore, Alice S, Ziegler, Regina G, Allen, Naomi E, Key, Timothy J, and Travis, Ruth C
Subjects: Cancer, Aging, Estrogen, Good Health and Well Being, Adult, Anthropometry, Behavior, Datasets as Topic, Gonadal Steroid Hormones, Humans, Male, Social Class, Young Adult, General Science & Technology
Abstract: IntroductionSex hormones have been implicated in the etiology of a number of diseases. To better understand disease etiology and the mechanisms of disease-risk factor associations, this analysis aimed to investigate the associations of anthropometric, sociodemographic and behavioural factors with a range of circulating sex hormones and sex hormone-binding globulin.MethodsStatistical analyses of individual participant data from 12,330 male controls aged 25-85 years from 25 studies involved in the Endogenous Hormones Nutritional Biomarkers and Prostate Cancer Collaborative Group. Analysis of variance was used to estimate geometric means adjusted for study and relevant covariates.ResultsOlder age was associated with higher concentrations of sex hormone-binding globulin and dihydrotestosterone and lower concentrations of dehydroepiandrosterone sulfate, free testosterone, androstenedione, androstanediol glucuronide and free estradiol. Higher body mass index was associated with higher concentrations of free estradiol, androstanediol glucuronide, estradiol and estrone and lower concentrations of dihydrotestosterone, testosterone, sex hormone-binding globulin, free testosterone, androstenedione and dehydroepiandrosterone sulfate. Taller height was associated with lower concentrations of androstenedione, testosterone, free testosterone and sex hormone-binding globulin and higher concentrations of androstanediol glucuronide. Current smoking was associated with higher concentrations of androstenedione, sex hormone-binding globulin and testosterone. Alcohol consumption was associated with higher concentrations of dehydroepiandrosterone sulfate, androstenedione and androstanediol glucuronide. East Asians had lower concentrations of androstanediol glucuronide and African Americans had higher concentrations of estrogens. Education and marital status were modestly associated with a small number of hormones.ConclusionCirculating sex hormones in men are strongly associated with age and body mass index, and to a lesser extent with smoking status and alcohol consumption.
Published: 2017

15. Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Author: Conti, David V., Darst, Burcu F., Moss, Lilit C., Saunders, Edward J., Sheng, Xin, Chou, Alisha, Schumacher, Fredrick R., Olama, Ali Amin Al, Benlloch, Sara, Dadaev, Tokhir, Brook, Mark N., Sahimi, Ali, Hoffmann, Thomas J., Takahashi, Atushi, Matsuda, Koichi, Momozawa, Yukihide, Fujita, Masashi, Muir, Kenneth, Lophatananon, Artitaya, Wan, Peggy, Le Marchand, Loic, Wilkens, Lynne R., Stevens, Victoria L., Gapstur, Susan M., Carter, Brian D., Schleutker, Johanna, Tammela, Teuvo L. J., Sipeky, Csilla, Auvinen, Anssi, Giles, Graham G., Southey, Melissa C., MacInnis, Robert J., Cybulski, Cezary, Wokołorczyk, Dominika, Lubiński, Jan, Neal, David E., Donovan, Jenny L., Hamdy, Freddie C., Martin, Richard M., Nordestgaard, Børge G., Nielsen, Sune F., Weischer, Maren, Bojesen, Stig E., Røder, Martin Andreas, Iversen, Peter, Batra, Jyotsna, Chambers, Suzanne, Moya, Leire, Horvath, Lisa, Clements, Judith A., Tilley, Wayne, Risbridger, Gail P., Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordström, Tobias, Pashayan, Nora, Dunning, Alison M., Ghoussaini, Maya, Travis, Ruth C., Key, Tim J., Riboli, Elio, Park, Jong Y., Sellers, Thomas A., Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie J., Mucci, Lorelei A., Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David J., Penney, Kathryn L., Turman, Constance, Tangen, Catherine M., Goodman, Phyllis J., Thompson, Jr., Ian M., Hamilton, Robert J., Fleshner, Neil E., Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet L., Ostrander, Elaine A., Geybels, Milan S., Koutros, Stella, Freeman, Laura E. Beane, Stampfer, Meir, Wolk, Alicja, Håkansson, Niclas, Andriole, Gerald L., Hoover, Robert N., Machiela, Mitchell J., Sørensen, Karina Dalsgaard, Borre, Michael, Blot, William J., Zheng, Wei, Yeboah, Edward D., Mensah, James E., Lu, Yong-Jie, Zhang, Hong-Wei, Feng, Ninghan, Mao, Xueying, Wu, Yudong, Zhao, Shan-Chao, Sun, Zan, Thibodeau, Stephen N., McDonnell, Shannon K., Schaid, Daniel J., West, Catharine M. L., Burnet, Neil, Barnett, Gill, Maier, Christiane, Schnoeller, Thomas, Luedeke, Manuel, Kibel, Adam S., Drake, Bettina F., Cussenot, Olivier, Cancel-Tassin, Géraldine, Menegaux, Florence, Truong, Thérèse, Koudou, Yves Akoli, John, Esther M., Grindedal, Eli Marie, Maehle, Lovise, Khaw, Kay-Tee, Ingles, Sue A., Stern, Mariana C., Vega, Ana, Gómez-Caamaño, Antonio, Fachal, Laura, Rosenstein, Barry S., Kerns, Sarah L., Ostrer, Harry, Teixeira, Manuel R., Paulo, Paula, Brandão, Andreia, Watya, Stephen, Lubwama, Alexander, Bensen, Jeannette T., Fontham, Elizabeth T. H., Mohler, James, Taylor, Jack A., Kogevinas, Manolis, Llorca, Javier, Castaño-Vinyals, Gemma, Cannon-Albright, Lisa, Teerlink, Craig C., Huff, Chad D., Strom, Sara S., Multigner, Luc, Blanchet, Pascal, Brureau, Laurent, Kaneva, Radka, Slavov, Chavdar, Mitev, Vanio, Leach, Robin J., Weaver, Brandi, Brenner, Hermann, Cuk, Katarina, Holleczek, Bernd, Saum, Kai-Uwe, Klein, Eric A., Hsing, Ann W., Kittles, Rick A., Murphy, Adam B., Logothetis, Christopher J., Kim, Jeri, Neuhausen, Susan L., Steele, Linda, Ding, Yuan Chun, Isaacs, William B., Nemesure, Barbara, Hennis, Anselm J. M., Carpten, John, Pandha, Hardev, Michael, Agnieszka, De Ruyck, Kim, De Meerleer, Gert, Ost, Piet, Xu, Jianfeng, Razack, Azad, Lim, Jasmine, Teo, Soo-Hwang, Newcomb, Lisa F., Lin, Daniel W., Fowke, Jay H., Neslund-Dudas, Christine, Rybicki, Benjamin A., Gamulin, Marija, Lessel, Davor, Kulis, Tomislav, Usmani, Nawaid, Singhal, Sandeep, Parliament, Matthew, Claessens, Frank, Joniau, Steven, Van den Broeck, Thomas, Gago-Dominguez, Manuela, Castelao, Jose Esteban, Martinez, Maria Elena, Larkin, Samantha, Townsend, Paul A., Aukim-Hastie, Claire, Bush, William S., Aldrich, Melinda C., Crawford, Dana C., Srivastava, Shiv, Cullen, Jennifer C., Petrovics, Gyorgy, Casey, Graham, Roobol, Monique J., Jenster, Guido, van Schaik, Ron H. N., Hu, Jennifer J., Sanderson, Maureen, Varma, Rohit, McKean-Cowdin, Roberta, Torres, Mina, Mancuso, Nicholas, Berndt, Sonja I., Van Den Eeden, Stephen K., Easton, Douglas F., Chanock, Stephen J., Cook, Michael B., Wiklund, Fredrik, Nakagawa, Hidewaki, Witte, John S., Eeles, Rosalind A., Kote-Jarai, Zsofia, and Haiman, Christopher A.
Published: 2021
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16. Female chromosome X mosaicism is age-related and preferentially affects the inactivated X chromosome

Author: Machiela, Mitchell J, Zhou, Weiyin, Karlins, Eric, Sampson, Joshua N, Freedman, Neal D, Yang, Qi, Hicks, Belynda, Dagnall, Casey, Hautman, Christopher, Jacobs, Kevin B, Abnet, Christian C, Aldrich, Melinda C, Amos, Christopher, Amundadottir, Laufey T, Arslan, Alan A, Beane-Freeman, Laura E, Berndt, Sonja I, Black, Amanda, Blot, William J, Bock, Cathryn H, Bracci, Paige M, Brinton, Louise A, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie E, Butler, Mary A, Canzian, Federico, Carreon, Tania, Chaffee, Kari G, Chang, I-Shou, Chatterjee, Nilanjan, Chen, Chu, Chen, Constance, Chen, Kexin, Chung, Charles C, Cook, Linda S, Bou, Marta Crous, Cullen, Michael, Davis, Faith G, De Vivo, Immaculata, Ding, Ti, Doherty, Jennifer, Duell, Eric J, Epstein, Caroline G, Fan, Jin-Hu, Figueroa, Jonine D, Fraumeni, Joseph F, Friedenreich, Christine M, Fuchs, Charles S, Gallinger, Steven, Gao, Yu-Tang, Gapstur, Susan M, Garcia-Closas, Montserrat, Gaudet, Mia M, Gaziano, J Michael, Giles, Graham G, Gillanders, Elizabeth M, Giovannucci, Edward L, Goldin, Lynn, Goldstein, Alisa M, Haiman, Christopher A, Hallmans, Goran, Hankinson, Susan E, Harris, Curtis C, Henriksson, Roger, Holly, Elizabeth A, Hong, Yun-Chul, Hoover, Robert N, Hsiung, Chao A, Hu, Nan, Hu, Wei, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Johansen, Christoffer, Khaw, Kay-Tee, Kim, Hee Nam, Kim, Yeul Hong, Kim, Young Tae, Klein, Alison P, Klein, Robert, Koh, Woon-Puay, Kolonel, Laurence N, Kooperberg, Charles, Kraft, Peter, Krogh, Vittorio, Kurtz, Robert C, LaCroix, Andrea, Lan, Qing, Landi, Maria Teresa, Le Marchand, Loic, Li, Donghui, Liang, Xiaolin, Liao, Linda M, Lin, Dongxin, Liu, Jianjun, Lissowska, Jolanta, Lu, Lingeng, Magliocco, Anthony M, and Malats, Nuria
Published: 2016

17. A Meta-analysis of Individual Participant Data Reveals an Association between Circulating Levels of IGF-I and Prostate Cancer Risk

Author: Travis, Ruth C, Appleby, Paul N, Martin, Richard M, Holly, Jeff MP, Albanes, Demetrius, Black, Amanda, Bueno-de-Mesquita, HB As, Chan, June M, Chen, Chu, Chirlaque, Maria-Dolores, Cook, Michael B, Deschasaux, Mélanie, Donovan, Jenny L, Ferrucci, Luigi, Galan, Pilar, Giles, Graham G, Giovannucci, Edward L, Gunter, Marc J, Habel, Laurel A, Hamdy, Freddie C, Helzlsouer, Kathy J, Hercberg, Serge, Hoover, Robert N, Janssen, Joseph AMJL, Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Metter, E Jeffrey, Mikami, Kazuya, Morris, Joan K, Neal, David E, Neuhouser, Marian L, Ozasa, Kotaro, Palli, Domenico, Platz, Elizabeth A, Pollak, Michael, Price, Alison J, Roobol, Monique J, Schaefer, Catherine, Schenk, Jeannette M, Severi, Gianluca, Stampfer, Meir J, Stattin, Pär, Tamakoshi, Akiko, Tangen, Catherine M, Touvier, Mathilde, Wald, Nicholas J, Weiss, Noel S, Ziegler, Regina G, Key, Timothy J, and Allen, Naomi E
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Prostate Cancer, Cancer, Urologic Diseases, Aged, Humans, Insulin-Like Growth Factor I, Male, Middle Aged, Prostatic Neoplasms, Risk Factors, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract: The role of insulin-like growth factors (IGF) in prostate cancer development is not fully understood. To investigate the association between circulating concentrations of IGFs (IGF-I, IGF-II, IGFBP-1, IGFBP-2, and IGFBP-3) and prostate cancer risk, we pooled individual participant data from 17 prospective and two cross-sectional studies, including up to 10,554 prostate cancer cases and 13,618 control participants. Conditional logistic regression was used to estimate the ORs for prostate cancer based on the study-specific fifth of each analyte. Overall, IGF-I, IGF-II, IGFBP-2, and IGFBP-3 concentrations were positively associated with prostate cancer risk (Ptrend all ≤ 0.005), and IGFBP-1 was inversely associated weakly with risk (Ptrend = 0.05). However, heterogeneity between the prospective and cross-sectional studies was evident (Pheterogeneity = 0.03), unless the analyses were restricted to prospective studies (with the exception of IGF-II, Pheterogeneity = 0.02). For prospective studies, the OR for men in the highest versus the lowest fifth of each analyte was 1.29 (95% confidence interval, 1.16-1.43) for IGF-I, 0.81 (0.68-0.96) for IGFBP-1, and 1.25 (1.12-1.40) for IGFBP-3. These associations did not differ significantly by time-to-diagnosis or tumor stage or grade. After mutual adjustment for each of the other analytes, only IGF-I remained associated with risk. Our collaborative study represents the largest pooled analysis of the relationship between prostate cancer risk and circulating concentrations of IGF-I, providing strong evidence that IGF-I is highly likely to be involved in prostate cancer development. Cancer Res; 76(8); 2288-300. ©2016 AACR.
Published: 2016

18. Usual adult occupation and risk of prostate cancer in West African men : the Ghana Prostate Study

Author: Adler, Colin, Friesen, Melissa C, Yeboah, Edward D, Tettey, Yao, Biritwum, Richard B, Adjei, Andrew A, Tay, Evelyn, Okyne, Victoria, Mensah, James E, Truelove, Ann, Yang, Baiyu, Kelly, Scott P, Zhou, Cindy Ke, McCullough, Lauren E, Pardo, Larissa, Hoover, Robert N, Hsing, Ann W, Cook, Michael B, and Koutros, Stella
Published: 2019

19. Maternal reproductive hormones and angiogenic factors in pregnancy and subsequent breast cancer risk

Author: Cornish, Rosie, Staff, Anne Cathrine, Boyd, Andy, Lawlor, Debbie A., Tretli, Steinar, Bradwin, Gary, McElrath, Thomas F., Hyer, Marianne, Hoover, Robert N., and Troisi, Rebecca
Published: 2019

20. Carotenoids, retinol, tocopherols, and prostate cancer risk: pooled analysis of 15 studies 1–3

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, Heliövaara, 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, Männistö, 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, Tjønneland, Anne, Touvier, Mathilde, Trichopoulou, Antonia, Weinstein, Stephanie J, Ziegler, Regina G, Zhou, Cindy Ke, Allen, Naomi E, Biomarkers, Endogenous Hormones Nutritional, and Group, Prostate Cancer Collaborative
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Urologic Diseases, Nutrition, Prostate Cancer, Cancer, Aging, Clinical Research, Adult, Biomarkers, Carotenoids, Case-Control Studies, Cohort Studies, Cross-Sectional Studies, Humans, Lycopene, Male, Meta-Analysis as Topic, Middle Aged, Neoplasm Grading, Neoplasm Staging, Observational Studies as Topic, Prospective Studies, Prostate, Prostatic Neoplasms, Risk Factors, Vitamin A, alpha-Tocopherol, prostate cancer, carotenoids, retinol, tocopherols, vitamin E, vitamin A, pooled analysis, nested case-control study, biomarkers, Endogenous Hormones Nutritional Biomarkers Prostate Cancer Collaborative Group, Engineering, Medical and Health Sciences, Nutrition & Dietetics, Clinical sciences, Nutrition and dietetics
Abstract: BackgroundIndividual 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.ObjectiveThe objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors.DesignPrincipal 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.ResultsData 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 α-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). γ-Tocopherol was not associated with risk.ConclusionsOverall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.
Published: 2015

21. Integration of multiethnic fine-mapping and genomic annotation to prioritize candidate functional SNPs at prostate cancer susceptibility regions

Author: Han, Ying, Hazelett, Dennis J, Wiklund, Fredrik, Schumacher, Fredrick R, Stram, Daniel O, Berndt, Sonja I, Wang, Zhaoming, Rand, Kristin A, Hoover, Robert N, Machiela, Mitchell J, Yeager, Merideth, Burdette, Laurie, Chung, Charles C, Hutchinson, Amy, Yu, Kai, Xu, Jianfeng, Travis, Ruth C, Key, Timothy J, Siddiq, Afshan, Canzian, Federico, Takahashi, Atsushi, Kubo, Michiaki, Stanford, Janet L, Kolb, Suzanne, Gapstur, Susan M, Diver, W Ryan, Stevens, Victoria L, Strom, Sara S, Pettaway, Curtis A, Olama, Ali Amin Al, Kote-Jarai, Zsofia, Eeles, Rosalind A, Yeboah, Edward D, Tettey, Yao, Biritwum, Richard B, Adjei, Andrew A, Tay, Evelyn, Truelove, Ann, Niwa, Shelley, Chokkalingam, Anand P, Isaacs, William B, Chen, Constance, Lindstrom, Sara, Le Marchand, Loic, Giovannucci, Edward L, Pomerantz, Mark, Long, Henry, Li, Fugen, Ma, Jing, Stampfer, Meir, John, Esther M, Ingles, Sue A, Kittles, Rick A, Murphy, Adam B, Blot, William J, Signorello, Lisa B, Zheng, Wei, Albanes, Demetrius, Virtamo, Jarmo, Weinstein, Stephanie, Nemesure, Barbara, Carpten, John, Leske, M Cristina, Wu, Suh-Yuh, Hennis, Anselm JM, Rybicki, Benjamin A, Neslund-Dudas, Christine, Hsing, Ann W, Chu, Lisa, Goodman, Phyllis J, Klein, Eric A, Zheng, S Lilly, Witte, John S, Casey, Graham, Riboli, Elio, Li, Qiyuan, Freedman, Matthew L, Hunter, David J, Gronberg, Henrik, Cook, Michael B, Nakagawa, Hidewaki, Kraft, Peter, Chanock, Stephen J, Easton, Douglas F, Henderson, Brian E, Coetzee, Gerhard A, Conti, David V, and Haiman, Christopher A
Subjects: Cancer, Human Genome, Biotechnology, Genetics, Urologic Diseases, Prostate Cancer, 2.1 Biological and endogenous factors, Aetiology, Asian People, Black People, Chromosome Mapping, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Hispanic or Latino, Humans, Linkage Disequilibrium, Male, Molecular Sequence Annotation, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Quantitative Trait Loci, White People, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract: Interpretation of biological mechanisms underlying genetic risk associations for prostate cancer is complicated by the relatively large number of risk variants (n = 100) and the thousands of surrogate SNPs in linkage disequilibrium. Here, we combined three distinct approaches: multiethnic fine-mapping, putative functional annotation (based upon epigenetic data and genome-encoded features), and expression quantitative trait loci (eQTL) analyses, in an attempt to reduce this complexity. We examined 67 risk regions using genotyping and imputation-based fine-mapping in populations of European (cases/controls: 8600/6946), African (cases/controls: 5327/5136), Japanese (cases/controls: 2563/4391) and Latino (cases/controls: 1034/1046) ancestry. Markers at 55 regions passed a region-specific significance threshold (P-value cutoff range: 3.9 × 10(-4)-5.6 × 10(-3)) and in 30 regions we identified markers that were more significantly associated with risk than the previously reported variants in the multiethnic sample. Novel secondary signals (P < 5.0 × 10(-6)) were also detected in two regions (rs13062436/3q21 and rs17181170/3p12). Among 666 variants in the 55 regions with P-values within one order of magnitude of the most-associated marker, 193 variants (29%) in 48 regions overlapped with epigenetic or other putative functional marks. In 11 of the 55 regions, cis-eQTLs were detected with nearby genes. For 12 of the 55 regions (22%), the most significant region-specific, prostate-cancer associated variant represented the strongest candidate functional variant based on our annotations; the number of regions increased to 20 (36%) and 27 (49%) when examining the 2 and 3 most significantly associated variants in each region, respectively. These results have prioritized subsets of candidate variants for downstream functional evaluation.
Published: 2015

22. Two susceptibility loci identified for prostate cancer aggressiveness.

Author: Berndt, Sonja I, Wang, Zhaoming, Yeager, Meredith, Alavanja, Michael C, Albanes, Demetrius, Amundadottir, Laufey, Andriole, Gerald, Beane Freeman, Laura, Campa, Daniele, Cancel-Tassin, Geraldine, Canzian, Federico, Cornu, Jean-Nicolas, Cussenot, Olivier, Diver, W Ryan, Gapstur, Susan M, Grönberg, Henrik, Haiman, Christopher A, Henderson, Brian, Hutchinson, Amy, Hunter, David J, Key, Timothy J, Kolb, Suzanne, Koutros, Stella, Kraft, Peter, Le Marchand, Loic, Lindström, Sara, Machiela, Mitchell J, Ostrander, Elaine A, Riboli, Elio, Schumacher, Fred, Siddiq, Afshan, Stanford, Janet L, Stevens, Victoria L, Travis, Ruth C, Tsilidis, Konstantinos K, Virtamo, Jarmo, Weinstein, Stephanie, Wilkund, Fredrik, Xu, Jianfeng, Lilly Zheng, S, Yu, Kai, Wheeler, William, Zhang, Han, African Ancestry Prostate Cancer GWAS Consortium, Sampson, Joshua, Black, Amanda, Jacobs, Kevin, Hoover, Robert N, Tucker, Margaret, and Chanock, Stephen J
Subjects: African Ancestry Prostate Cancer GWAS Consortium, Humans, Prostatic Neoplasms, Neoplasm Invasiveness, Genetic Predisposition to Disease, Case-Control Studies, Male, Genetic Loci, Neoplasm Grading
Abstract: Most men diagnosed with prostate cancer will experience indolent disease; hence, discovering genetic variants that distinguish aggressive from nonaggressive prostate cancer is of critical clinical importance for disease prevention and treatment. In a multistage, case-only genome-wide association study of 12,518 prostate cancer cases, we identify two loci associated with Gleason score, a pathological measure of disease aggressiveness: rs35148638 at 5q14.3 (RASA1, P=6.49 × 10(-9)) and rs78943174 at 3q26.31 (NAALADL2, P=4.18 × 10(-8)). In a stratified case-control analysis, the SNP at 5q14.3 appears specific for aggressive prostate cancer (P=8.85 × 10(-5)) with no association for nonaggressive prostate cancer compared with controls (P=0.57). The proximity of these loci to genes involved in vascular disease suggests potential biological mechanisms worthy of further investigation.
Published: 2015

23. Opportunities—And Hard Work—Ahead

Author: Hoover, Robert N and Chanock, Stephen J
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biomedical Research, Epigenomics, Gene Expression Profiling, Genetic Predisposition to Disease, Genomics, Humans, Metabolomics, Neoplasms, Proteomics, Signal Transduction, Transcriptome, Clinical Research, Human Genome, Brain Cancer, Genetics, Cancer, Brain Disorders, Neurosciences, Rare Diseases, Adult, Aged, Brain Neoplasms, Exome, Female, Germ-Line Mutation, Glioma, Male, Middle Aged, Oligodendroglioma, Pedigree, Shelterin Complex, Telomere-Binding Proteins, Gliogene Consortium, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract: Gliomas are the most common brain tumor, with several histological subtypes of various malignancy grade. The genetic contribution to familial glioma is not well understood. Using whole exome sequencing of 90 individuals from 55 families, we identified two families with mutations in POT1 (p.G95C, p.E450X), a member of the telomere shelterin complex, shared by both affected individuals in each family and predicted to impact DNA binding and TPP1 binding, respectively. Validation in a separate cohort of 264 individuals from 246 families identified an additional mutation in POT1 (p.D617Efs), also predicted to disrupt TPP1 binding. All families with POT1 mutations had affected members with oligodendroglioma, a specific subtype of glioma more sensitive to irradiation. These findings are important for understanding the origin of glioma and could have importance for the future diagnostics and treatment of glioma.
Published: 2014

24. Reproductive and hormone-related outcomes in women whose mothers were exposed in utero to diethylstilbestrol (DES): A report from the US National Cancer Institute DES Third Generation Study

Author: Titus, Linda, Hatch, Elizabeth E., Drake, Keith M., Parker, Samantha E., Hyer, Marianne, Palmer, Julie R., Strohsnitter, William C., Adam, Ervin, Herbst, Arthur L., Huo, Dezheng, Hoover, Robert N., and Troisi, Rebecca
Published: 2019
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25. High Prevalence of Screen Detected Prostate Cancer in West Africans: Implications for Racial Disparity of Prostate Cancer

Author: Hsing, Ann W, Yeboah, Edward, Biritwum, Richard, Tettey, Yao, De Marzo, Angelo M, Adjei, Andrew, Netto, George J, Yu, Kai, Li, Yan, Chokkalingam, Anand P, Chu, Lisa W, Chia, David, Partin, Alan, Thompson, Ian M, Quraishi, Sabah M, Niwa, Shelley, Tarone, Robert, and Hoover, Robert N
Subjects: Clinical Research, Prostate Cancer, Urologic Diseases, Genetics, Cancer, Aging, Prevention, Black or African American, Aged, Black People, Ghana, Humans, Male, Middle Aged, Prevalence, Prostate-Specific Antigen, Prostatic Neoplasms, Africa, African Americans, mass screening, prostate-specific antigen, prostatic neoplasms
Abstract: PurposeTo our knowledge the reasons for the high rates of prostate cancer in black American men are unknown. Genetic and lifestyle factors have been implicated. Better understanding of prostate cancer rates in West African men would help clarify why black American men have such high rates since the groups share genetic ancestry and yet have different lifestyles and screening practices. To estimate the prostate cancer burden in West African men we performed a population based screening study with biopsy confirmation in Ghana.Materials and methodsWe randomly selected 1,037 healthy men 50 to 74 years old from Accra, Ghana for prostate cancer screening with prostate specific antigen testing and digital rectal examination. Men with a positive screen result (positive digital rectal examination or prostate specific antigen greater than 2.5 ng/ml) underwent transrectal ultrasound guided biopsies.ResultsOf the 1,037 men 154 (14.9%) had a positive digital rectal examination and 272 (26.2%) had prostate specific antigen greater than 2.5 ng/ml, including 166 with prostate specific antigen greater than 4.0 ng/ml. A total of 352 men (33.9%) had a positive screen by prostate specific antigen or digital rectal examination and 307 (87%) underwent biopsy. Of these men 73 were confirmed to have prostate cancer, yielding a 7.0% screen detected prostate cancer prevalence (65 patients), including 5.8% with prostate specific antigen greater than 4.0 ng/ml.ConclusionsIn this relatively unscreened population in Africa the screen detected prostate cancer prevalence is high, suggesting a possible role of genetics in prostate cancer etiology and the disparity in prostate cancer risk between black and white American men. Further studies are needed to confirm the high prostate cancer burden in African men and the role of genetics in prostate cancer etiology.
Published: 2014

26. Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men.

Author: Finkle, William D, Greenland, Sander, Ridgeway, Gregory K, Adams, John L, Frasco, Melissa A, Cook, Michael B, Fraumeni, Joseph F, and Hoover, Robert N
Subjects: Humans, Myocardial Infarction, Sulfones, Piperazines, Carbolines, Purines, Testosterone, Risk, Age Factors, Aged, Middle Aged, Male, Prescription Drugs, Phosphodiesterase 5 Inhibitors, Sildenafil Citrate, Tadalafil, General Science & Technology
Abstract: BackgroundAn association between testosterone therapy (TT) and cardiovascular disease has been reported and TT use is increasing rapidly.MethodsWe conducted a cohort study of the risk of acute non-fatal myocardial infarction (MI) following an initial TT prescription (N = 55,593) in a large health-care database. We compared the incidence rate of MI in the 90 days following the initial prescription (post-prescription interval) with the rate in the one year prior to the initial prescription (pre-prescription interval) (post/pre). We also compared post/pre rates in a cohort of men prescribed phosphodiesterase type 5 inhibitors (PDE5I; sildenafil or tadalafil, N = 167,279), and compared TT prescription post/pre rates with the PDE5I post/pre rates, adjusting for potential confounders using doubly robust estimation.ResultsIn all subjects, the post/pre-prescription rate ratio (RR) for TT prescription was 1.36 (1.03, 1.81). In men aged 65 years and older, the RR was 2.19 (1.27, 3.77) for TT prescription and 1.15 (0.83, 1.59) for PDE5I, and the ratio of the rate ratios (RRR) for TT prescription relative to PDE5I was 1.90 (1.04, 3.49). The RR for TT prescription increased with age from 0.95 (0.54, 1.67) for men under age 55 years to 3.43 (1.54, 7.56) for those aged ≥ 75 years (p trend = 0.03), while no trend was seen for PDE5I (p trend = 0.18). In men under age 65 years, excess risk was confined to those with a prior history of heart disease, with RRs of 2.90 (1.49, 5.62) for TT prescription and 1.40 (0.91, 2.14) for PDE5I, and a RRR of 2.07 (1.05, 4.11).DiscussionIn older men, and in younger men with pre-existing diagnosed heart disease, the risk of MI following initiation of TT prescription is substantially increased.
Published: 2014

27. Transforming Epidemiology for 21st Century Medicine and Public Health

Author: Khoury, Muin J, Lam, Tram Kim, Ioannidis, John PA, Hartge, Patricia, Spitz, Margaret R, Buring, Julie E, Chanock, Stephen J, Croyle, Robert T, Goddard, Katrina A, Ginsburg, Geoffrey S, Herceg, Zdenko, Hiatt, Robert A, Hoover, Robert N, Hunter, David J, Kramer, Barnet S, Lauer, Michael S, Meyerhardt, Jeffrey A, Olopade, Olufunmilayo I, Palmer, Julie R, Sellers, Thomas A, Seminara, Daniela, Ransohoff, David F, Rebbeck, Timothy R, Tourassi, Georgia, Winn, Deborah M, Zauber, Ann, and Schully, Sheri D
Subjects: Epidemiology, Public Health, Health Sciences, Cancer, Clinical Research, Generic health relevance, Good Health and Well Being, Biomedical Research, Epidemiologic Studies, Guidelines as Topic, History, 21st Century, Humans, Medical Oncology, National Cancer Institute (U.S.), Neoplasms, United States, National Cancer Institute, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract: In 2012, the National Cancer Institute (NCI) engaged the scientific community to provide a vision for cancer epidemiology in the 21st century. Eight overarching thematic recommendations, with proposed corresponding actions for consideration by funding agencies, professional societies, and the research community emerged from the collective intellectual discourse. The themes are (i) extending the reach of epidemiology beyond discovery and etiologic research to include multilevel analysis, intervention evaluation, implementation, and outcomes research; (ii) transforming the practice of epidemiology by moving toward more access and sharing of protocols, data, metadata, and specimens to foster collaboration, to ensure reproducibility and replication, and accelerate translation; (iii) expanding cohort studies to collect exposure, clinical, and other information across the life course and examining multiple health-related endpoints; (iv) developing and validating reliable methods and technologies to quantify exposures and outcomes on a massive scale, and to assess concomitantly the role of multiple factors in complex diseases; (v) integrating "big data" science into the practice of epidemiology; (vi) expanding knowledge integration to drive research, policy, and practice; (vii) transforming training of 21st century epidemiologists to address interdisciplinary and translational research; and (viii) optimizing the use of resources and infrastructure for epidemiologic studies. These recommendations can transform cancer epidemiology and the field of epidemiology, in general, by enhancing transparency, interdisciplinary collaboration, and strategic applications of new technologies. They should lay a strong scientific foundation for accelerated translation of scientific discoveries into individual and population health benefits.
Published: 2013

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

Author: Leenders, Max, Bhattacharjee, Samsiddhi, Vineis, Paolo, Stevens, Victoria, Bueno-de-Mesquita, H Bas, Shu, Xiao-Ou, Amundadottir, Laufey, Gross, Myron, Tobias, Geoffrey S, Wactawski-Wende, Jean, Arslan, Alan A, Duell, Eric J, Fuchs, Charles S, Gallinger, Steven, Hartge, Patricia, Hoover, Robert N, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, Kooperberg, Charles, LaCroix, Andrea, Li, Donghui, Mandelson, Margaret T, Olson, Sara H, Petersen, Gloria, Risch, Harvey A, Yu, Kai, Wolpin, Brian M, Zheng, Wei, Agalliu, Ilir, Albanes, Demetrius, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Buring, Julie E, Canzian, Federico, Chang, Kenneth, Chanock, Stephen J, Cotterchio, Michelle, Gaziano, J Michael, Giovanucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hoffman-Bolton, Judith A, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin B, Jenab, Mazda, Khaw, Kay-Tee, Kraft, Peter, Krogh, Vittorio, Kurtz, Robert C, McWilliams, Robert R, Mendelsohn, Julie B, Patel, Alpa V, Rabe, Kari G, Riboli, Elio, Tjønneland, Anne, Trichopoulos, Dimitrios, Virtamo, Jarmo, Visvanathan, Kala, Elena, Joanne W, Yu, Herbert, Zeleniuch-Jacquotte, Anne, and Stolzenberg-Solomon, Rachael Z
Subjects: Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Cancer, Digestive Diseases, Genetics, Pancreatic Cancer, Prevention, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Carbon, Case-Control Studies, Cohort Studies, Germ-Line Mutation, Humans, Pancreatic Neoplasms, Polymorphism, Single Nucleotide, United States, Pancreatic cancer, One-carbon metabolism, Polymorphisms, Biomarkers, Public Health and Health Services, Oncology and carcinogenesis
Abstract: PurposeThe evidence of a relation between folate intake and one-carbon metabolism (OCM) with pancreatic cancer (PanCa) is inconsistent. In this study, the association between genes and single-nucleotide polymorphisms (SNPs) related to OCM and PanCa was assessed.MethodsUsing biochemical knowledge of the OCM pathway, we identified thirty-seven genes and 834 SNPs to examine in association with PanCa. Our study included 1,408 cases and 1,463 controls nested within twelve cohorts (PanScan). The ten SNPs and five genes with lowest p values (
Published: 2013

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

Author: Elena, Joanne W, Steplowski, Emily, Yu, Kai, Hartge, Patricia, Tobias, Geoffrey S, Brotzman, Michelle J, Chanock, Stephen J, Stolzenberg-Solomon, Rachael Z, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Petersen, Gloria, Zheng, Wei, Albanes, Demetrius, Allen, Naomi E, Amundadottir, Laufey, Bao, Ying, Boeing, Heiner, Boutron-Ruault, Marie-Christine, Buring, Julie E, Gaziano, J Michael, Giovannucci, Edward L, Duell, Eric J, Hallmans, Göran, Howard, Barbara V, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin B, Kooperberg, Charles, Kraft, Peter, Mendelsohn, Julie B, Michaud, Dominique S, Palli, Domenico, Phillips, Lawrence S, Overvad, Kim, Patel, Alpa V, Sansbury, Leah, Shu, Xiao-Ou, Simon, Michael S, Slimani, Nadia, Trichopoulos, Dimitrios, Visvanathan, Kala, Virtamo, Jarmo, Wolpin, Brian M, Zeleniuch-Jacquotte, Anne, Fuchs, Charles S, Hoover, Robert N, and Gross, Myron
Subjects: Biomedical and Clinical Sciences, Epidemiology, Health Services and Systems, Health Sciences, Oncology and Carcinogenesis, Rare Diseases, Cancer, Pancreatic Cancer, Prevention, Digestive Diseases, Clinical Research, Diabetes, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Good Health and Well Being, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Diabetes Complications, Diabetes Mellitus, Female, Humans, Male, Middle Aged, Pancreatic Neoplasms, Risk Factors, Public Health and Health Services, Oncology and carcinogenesis
Abstract: PurposeDiabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan).MethodsThe pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (
Published: 2013

30. Genome-wide association study of germline variants and breast cancer-specific mortality

Author: Escala-Garcia, Maria, Guo, Qi, Dörk, Thilo, Canisius, Sander, Keeman, Renske, Dennis, Joe, Beesley, Jonathan, Lecarpentier, Julie, Bolla, Manjeet K., Wang, Qin, Abraham, Jean, Andrulis, Irene L., Anton-Culver, Hoda, Arndt, Volker, Auer, Paul L., Beckmann, Matthias W., Behrens, Sabine, Benitez, Javier, Bermisheva, Marina, Bernstein, Leslie, Blomqvist, Carl, Boeckx, Bram, Bojesen, Stig E., Bonanni, Bernardo, Børresen-Dale, Anne-Lise, Brauch, Hiltrud, Brenner, Hermann, Brentnall, Adam, Brinton, Louise, Broberg, Per, Brock, Ian W., Brucker, Sara Y., Burwinkel, Barbara, Caldas, Carlos, Caldés, Trinidad, Campa, Daniele, Canzian, Federico, Carracedo, Angel, Carter, Brian D., Castelao, Jose E., Chang-Claude, Jenny, Chanock, Stephen J., Chenevix-Trench, Georgia, Cheng, Ting-Yuan David, Chin, Suet-Feung, Clarke, Christine L., NBCS Collaborators, Cordina-Duverger, Emilie, Couch, Fergus J., Cox, David G., Cox, Angela, Cross, Simon S., Czene, Kamila, Daly, Mary B., Devilee, Peter, Dunn, Janet A., Dunning, Alison M., Durcan, Lorraine, Dwek, Miriam, Earl, Helena M., Ekici, Arif B., Eliassen, A. Heather, Ellberg, Carolina, Engel, Christoph, Eriksson, Mikael, Evans, D. Gareth, Figueroa, Jonine, Flesch-Janys, Dieter, Flyger, Henrik, Gabrielson, Marike, Gago-Dominguez, Manuela, Galle, Eva, Gapstur, Susan M., García-Closas, Montserrat, García-Sáenz, José A., Gaudet, Mia M., George, Angela, Georgoulias, Vassilios, Giles, Graham G., Glendon, Gord, Goldgar, David E., González-Neira, Anna, Alnæs, Grethe I. Grenaker, Grip, Mervi, Guénel, Pascal, Haeberle, Lothar, Hahnen, Eric, Haiman, Christopher A., Håkansson, Niclas, Hall, Per, Hamann, Ute, Hankinson, Susan, Harkness, Elaine F., Harrington, Patricia A., Hart, Steven N., Hartikainen, Jaana M., Hein, Alexander, Hillemanns, Peter, Hiller, Louise, Holleczek, Bernd, Hollestelle, Antoinette, Hooning, Maartje J., Hoover, Robert N., Hopper, John L., Howell, Anthony, Huang, Guanmengqian, Humphreys, Keith, Hunter, David J., Janni, Wolfgang, John, Esther M., Jones, Michael E., Jukkola-Vuorinen, Arja, Jung, Audrey, Kaaks, Rudolf, Kabisch, Maria, Kaczmarek, Katarzyna, Kerin, Michael J., Khan, Sofia, Khusnutdinova, Elza, Kiiski, Johanna I., Kitahara, Cari M., Knight, Julia A., Ko, Yon-Dschun, Koppert, Linetta B., Kosma, Veli-Matti, Kraft, Peter, Kristensen, Vessela N., Krüger, Ute, Kühl, Tabea, Lambrechts, Diether, Le Marchand, Loic, Lee, Eunjung, Lejbkowicz, Flavio, Li, Lian, Lindblom, Annika, Lindström, Sara, Linet, Martha, Lissowska, Jolanta, Lo, Wing-Yee, Loibl, Sibylle, Lubiński, Jan, Lux, Michael P., MacInnis, Robert J., Maierthaler, Melanie, Maishman, Tom, Makalic, Enes, Mannermaa, Arto, Manoochehri, Mehdi, Manoukian, Siranoush, Margolin, Sara, Martinez, Maria Elena, Mavroudis, Dimitrios, McLean, Catriona, Meindl, Alfons, Middha, Pooja, Miller, Nicola, Milne, Roger L., Moreno, Fernando, Mulligan, Anna Marie, Mulot, Claire, Nassir, Rami, Neuhausen, Susan L., Newman, William T., Nielsen, Sune F., Nordestgaard, Børge G., Norman, Aaron, Olsson, Håkan, Orr, Nick, Pankratz, V. Shane, Park-Simon, Tjoung-Won, Perez, Jose I. A., Pérez-Barrios, Clara, Peterlongo, Paolo, Petridis, Christos, Pinchev, Mila, Prajzendanc, Karoliona, Prentice, Ross, Presneau, Nadege, Prokofieva, Darya, Pylkäs, Katri, Rack, Brigitte, Radice, Paolo, Ramachandran, Dhanya, Rennert, Gadi, Rennert, Hedy S., Rhenius, Valerie, Romero, Atocha, Roylance, Rebecca, Saloustros, Emmanouil, Sawyer, Elinor J., Schmidt, Daniel F., Schmutzler, Rita K., Schneeweiss, Andreas, Schoemaker, Minouk J., Schumacher, Fredrick, Schwentner, Lukas, Scott, Rodney J., Scott, Christopher, Seynaeve, Caroline, Shah, Mitul, Simard, Jacques, Smeets, Ann, Sohn, Christof, Southey, Melissa C., Swerdlow, Anthony J., Talhouk, Aline, Tamimi, Rulla M., Tapper, William J., Teixeira, Manuel R., Tengström, Maria, Terry, Mary Beth, Thöne, Kathrin, Tollenaar, Rob A. E. M., Tomlinson, Ian, Torres, Diana, Truong, Thérèse, Turman, Constance, Turnbull, Clare, Ulmer, Hans-Ulrich, Untch, Michael, Vachon, Celine, van Asperen, Christi J., van den Ouweland, Ans M. W., van Veen, Elke M., Wendt, Camilla, Whittemore, Alice S., Willett, Walter, Winqvist, Robert, Wolk, Alicja, Yang, Xiaohong R., Zhang, Yan, Easton, Douglas F., Fasching, Peter A., Nevanlinna, Heli, Eccles, Diana M., Pharoah, Paul D. P., and Schmidt, Marjanka K.
Published: 2019
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31. A meta-analysis of genome-wide association studies of breast cancer identifies two novel susceptibility loci at 6q14 and 20q11

Author: Siddiq, Afshan, Couch, Fergus J, Chen, Gary K, Lindström, Sara, Eccles, Diana, Millikan, Robert C, Michailidou, Kyriaki, Stram, Daniel O, Beckmann, Lars, Rhie, Suhn Kyong, Ambrosone, Christine B, Aittomäki, Kristiina, Amiano, Pilar, Apicella, Carmel, Investigators, Australian Breast Cancer Tissue Bank, Baglietto, Laura, Bandera, Elisa V, Beckmann, Matthias W, Berg, Christine D, Bernstein, Leslie, Blomqvist, Carl, Brauch, Hiltrud, Brinton, Louise, Bui, Quang M, Buring, Julie E, Buys, Saundra S, Campa, Daniele, Carpenter, Jane E, Chasman, Daniel I, Chang-Claude, Jenny, Chen, Constance, Clavel-Chapelon, Françoise, Cox, Angela, Cross, Simon S, Czene, Kamila, Deming, Sandra L, Diasio, Robert B, Diver, W Ryan, Dunning, Alison M, Durcan, Lorraine, Ekici, Arif B, Fasching, Peter A, Study, Familial Breast Cancer, Feigelson, Heather Spencer, Fejerman, Laura, Figueroa, Jonine D, Fletcher, Olivia, Flesch-Janys, Dieter, Gaudet, Mia M, Consortium, The GENICA, Gerty, Susan M, Rodriguez-Gil, Jorge L, Giles, Graham G, van Gils, Carla H, Godwin, Andrew K, Graham, Nikki, Greco, Dario, Hall, Per, Hankinson, Susan E, Hartmann, Arndt, Hein, Rebecca, Heinz, Judith, Hoover, Robert N, Hopper, John L, Hu, Jennifer J, Huntsman, Scott, Ingles, Sue A, Irwanto, Astrid, Isaacs, Claudine, Jacobs, Kevin B, John, Esther M, Justenhoven, Christina, Kaaks, Rudolf, Kolonel, Laurence N, Coetzee, Gerhard A, Lathrop, Mark, Le Marchand, Loic, Lee, Adam M, Lee, I-Min, Lesnick, Timothy, Lichtner, Peter, Liu, Jianjun, Lund, Eiliv, Makalic, Enes, Martin, Nicholas G, McLean, Catriona A, Meijers-Heijboer, Hanne, Meindl, Alfons, Miron, Penelope, Monroe, Kristine R, Montgomery, Grant W, Müller-Myhsok, Bertram, Nickels, Stefan, Nyante, Sarah J, Olswold, Curtis, Overvad, Kim, Palli, Domenico, Park, Daniel J, Palmer, Julie R, and Pathak, Harsh
Subjects: Biological Sciences, Genetics, Clinical Research, Aging, Human Genome, Breast Cancer, Cancer, Aetiology, 2.1 Biological and endogenous factors, Breast Neoplasms, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Receptors, Estrogen, Australian Breast Cancer Tissue Bank Investigators, Familial Breast Cancer Study, GENICA Consortium, Medical and Health Sciences, Genetics & Heredity
Abstract: Genome-wide association studies (GWAS) of breast cancer defined by hormone receptor status have revealed loci contributing to susceptibility of estrogen receptor (ER)-negative subtypes. To identify additional genetic variants for ER-negative breast cancer, we conducted the largest meta-analysis of ER-negative disease to date, comprising 4754 ER-negative cases and 31 663 controls from three GWAS: NCI Breast and Prostate Cancer Cohort Consortium (BPC3) (2188 ER-negative cases; 25 519 controls of European ancestry), Triple Negative Breast Cancer Consortium (TNBCC) (1562 triple negative cases; 3399 controls of European ancestry) and African American Breast Cancer Consortium (AABC) (1004 ER-negative cases; 2745 controls). We performed in silico replication of 86 SNPs at P ≤ 1 × 10(-5) in an additional 11 209 breast cancer cases (946 with ER-negative disease) and 16 057 controls of Japanese, Latino and European ancestry. We identified two novel loci for breast cancer at 20q11 and 6q14. SNP rs2284378 at 20q11 was associated with ER-negative breast cancer (combined two-stage OR = 1.16; P = 1.1 × 10(-8)) but showed a weaker association with overall breast cancer (OR = 1.08, P = 1.3 × 10(-6)) based on 17 869 cases and 43 745 controls and no association with ER-positive disease (OR = 1.01, P = 0.67) based on 9965 cases and 22 902 controls. Similarly, rs17530068 at 6q14 was associated with breast cancer (OR = 1.12; P = 1.1 × 10(-9)), and with both ER-positive (OR = 1.09; P = 1.5 × 10(-5)) and ER-negative (OR = 1.16, P = 2.5 × 10(-7)) disease. We also confirmed three known loci associated with ER-negative (19p13) and both ER-negative and ER-positive breast cancer (6q25 and 12p11). Our results highlight the value of large-scale collaborative studies to identify novel breast cancer risk loci.
Published: 2012

32. Genome-wide association study of glioma and meta-analysis

Author: Rajaraman, Preetha, Melin, Beatrice S, Wang, Zhaoming, McKean-Cowdin, Roberta, Michaud, Dominique S, Wang, Sophia S, Bondy, Melissa, Houlston, Richard, Jenkins, Robert B, Wrensch, Margaret, Yeager, Meredith, Ahlbom, Anders, Albanes, Demetrius, Andersson, Ulrika, Freeman, Laura E Beane, Buring, Julie E, Butler, Mary Ann, Braganza, Melissa, Carreon, Tania, Feychting, Maria, Fleming, Sarah J, Gapstur, Susan M, Gaziano, J Michael, Giles, Graham G, Hallmans, Goran, Henriksson, Roger, Hoffman-Bolton, Judith, Inskip, Peter D, Johansen, Christoffer, Kitahara, Cari M, Lathrop, Mark, Liu, Chenwei, Le Marchand, Loic, Linet, Martha S, Lonn, Stefan, Peters, Ulrike, Purdue, Mark P, Rothman, Nathaniel, Ruder, Avima M, Sanson, Marc, Sesso, Howard D, Severi, Gianluca, Shu, Xiao-Ou, Simon, Matthias, Stampfer, Meir, Stevens, Victoria L, Visvanathan, Kala, White, Emily, Wolk, Alicja, Zeleniuch-Jacquotte, Anne, Zheng, Wei, Decker, Paul, Enciso-Mora, Victor, Fridley, Brooke, Gao, Yu-Tang, Kosel, Matthew, Lachance, Daniel H, Lau, Ching, Rice, Terri, Swerdlow, Anthony, Wiemels, Joseph L, Wiencke, John K, Shete, Sanjay, Xiang, Yong-Bing, Xiao, Yuanyuan, Hoover, Robert N, Fraumeni, Joseph F, Chatterjee, Nilanjan, Hartge, Patricia, and Chanock, Stephen J
Subjects: Biological Sciences, Biomedical and Clinical Sciences, Genetics, Clinical Research, Brain Disorders, Prevention, Brain Cancer, Neurosciences, Cancer, Human Genome, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Aged, Brain Neoplasms, Case-Control Studies, Cohort Studies, Cyclin-Dependent Kinase Inhibitor p15, DNA Helicases, Female, Genome-Wide Association Study, Glioblastoma, Glioma, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Telomerase, Complementary and Alternative Medicine, Paediatrics and Reproductive Medicine, Genetics & Heredity, Reproductive medicine
Abstract: Gliomas account for approximately 80 % of all primary malignant brain tumors and, despite improvements in clinical care over the last 20 years, remain among the most lethal tumors, underscoring the need for gaining new insights that could translate into clinical advances. Recent genome-wide association studies (GWAS) have identified seven new susceptibility regions. We conducted a new independent GWAS of glioma using 1,856 cases and 4,955 controls (from 14 cohort studies, 3 case-control studies, and 1 population-based case-only study) and found evidence of strong replication for three of the seven previously reported associations at 20q13.33 (RTEL), 5p15.33 (TERT), and 9p21.3 (CDKN2BAS), and consistent association signals for the remaining four at 7p11.2 (EGFR both loci), 8q24.21 (CCDC26) and 11q23.3 (PHLDB1). The direction and magnitude of the signal were consistent for samples from cohort and case-control studies, but the strength of the association was more pronounced for loci rs6010620 (20q,13.33; RTEL) and rs2736100 (5p15.33, TERT) in cohort studies despite the smaller number of cases in this group, likely due to relatively more higher grade tumors being captured in the cohort studies. We further examined the 85 most promising single nucleotide polymorphism (SNP) markers identified in our study in three replication sets (5,015 cases and 11,601 controls), but no new markers reached genome-wide significance. Our findings suggest that larger studies focusing on novel approaches as well as specific tumor subtypes or subgroups will be required to identify additional common susceptibility loci for glioma risk.
Published: 2012

33. Secondary Sex Ratio among Women Exposed to Diethylstilbestrol in Utero

Author: Wise, Lauren A., Palmer, Julie R., Hatch, Elizabeth E., Troisi, Rebecca, Titus-Ernstoff, Linda, Herbst, Arthur L., Kaufman, Raymond, Noller, Kenneth L., and Hoover, Robert N.
Published: 2007

34. Pathway analysis of genome-wide association study data highlights pancreatic development genes as susceptibility factors for pancreatic cancer.

Author: Li, Donghui, Duell, Eric J, Yu, Kai, Risch, Harvey A, Olson, Sara H, Kooperberg, Charles, Wolpin, Brian M, Jiao, Li, Dong, Xiaoqun, Wheeler, Bill, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Fuchs, Charles S, Gallinger, Steven, Gross, Myron, Hartge, Patricia, Hoover, Robert N, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, LaCroix, Andrea, Mandelson, Margaret T, Petersen, Gloria, Zheng, Wei, Agalliu, Ilir, Albanes, Demetrius, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Buring, Julie E, Canzian, Federico, Chang, Kenneth, Chanock, Stephen J, Cotterchio, Michelle, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hoffman Bolton, Judith A, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin B, Jenab, Mazda, Khaw, Kay-Tee, Kraft, Peter, Krogh, Vittorio, Kurtz, Robert C, McWilliams, Robert R, Mendelsohn, Julie B, Patel, Alpa V, Rabe, Kari G, Riboli, Elio, Shu, Xiao-Ou, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Virtamo, Jarmo, Visvanathan, Kala, Watters, Joanne, Yu, Herbert, Zeleniuch-Jacquotte, Anne, Amundadottir, Laufey, and Stolzenberg-Solomon, Rachael Z
Subjects: Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Polymorphism, Single Nucleotide, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract: Four loci have been associated with pancreatic cancer through genome-wide association studies (GWAS). Pathway-based analysis of GWAS data is a complementary approach to identify groups of genes or biological pathways enriched with disease-associated single-nucleotide polymorphisms (SNPs) whose individual effect sizes may be too small to be detected by standard single-locus methods. We used the adaptive rank truncated product method in a pathway-based analysis of GWAS data from 3851 pancreatic cancer cases and 3934 control participants pooled from 12 cohort studies and 8 case-control studies (PanScan). We compiled 23 biological pathways hypothesized to be relevant to pancreatic cancer and observed a nominal association between pancreatic cancer and five pathways (P < 0.05), i.e. pancreatic development, Helicobacter pylori lacto/neolacto, hedgehog, Th1/Th2 immune response and apoptosis (P = 2.0 × 10(-6), 1.6 × 10(-5), 0.0019, 0.019 and 0.023, respectively). After excluding previously identified genes from the original GWAS in three pathways (NR5A2, ABO and SHH), the pancreatic development pathway remained significant (P = 8.3 × 10(-5)), whereas the others did not. The most significant genes (P < 0.01) in the five pathways were NR5A2, HNF1A, HNF4G and PDX1 for pancreatic development; ABO for H.pylori lacto/neolacto; SHH for hedgehog; TGFBR2 and CCL18 for Th1/Th2 immune response and MAPK8 and BCL2L11 for apoptosis. Our results provide a link between inherited variation in genes important for pancreatic development and cancer and show that pathway-based approaches to analysis of GWAS data can yield important insights into the collective role of genetic risk variants in cancer.
Published: 2012

35. Variant ABO Blood Group Alleles, Secretor Status, and Risk of Pancreatic Cancer: Results from the Pancreatic Cancer Cohort Consortium

Author: Wolpin, Brian M, Kraft, Peter, Xu, Mousheng, Steplowski, Emily, Olsson, Martin L, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Petersen, Gloria, Stolzenberg-Solomon, Rachael Z, Zheng, Wei, Albanes, Demetrius, Allen, Naomi E, Amundadottir, Laufey, Austin, Melissa A, Boutron-Ruault, Marie-Christine, Buring, Julie E, Canzian, Federico, Chanock, Stephen J, Gaziano, J Michael, Giovannucci, Edward L, Hallmans, Göran, Hankinson, Susan E, Hoover, Robert N, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin B, Kooperberg, Charles, Mendelsohn, Julie B, Michaud, Dominique S, Overvad, Kim, Patel, Alpa V, Sanchéz, Maria-José, Sansbury, Leah, Shu, Xiao-Ou, Slimani, Nadia, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Vineis, Paolo, Visvanathan, Kala, Virtamo, Jarmo, Wactawski-Wende, Jean, Watters, Joanne, Yu, Kai, Zeleniuch-Jacquotte, Anne, Hartge, Patricia, and Fuchs, Charles S
Subjects: Digestive Diseases, Cancer, Clinical Research, Genetics, Rare Diseases, Pancreatic Cancer, Prevention, Human Genome, Aetiology, 2.1 Biological and endogenous factors, ABO Blood-Group System, Alleles, Cohort Studies, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Glycosyltransferases, Humans, Odds Ratio, Pancreatic Neoplasms, Phenotype, Polymorphism, Single Nucleotide, Medical and Health Sciences, Epidemiology
Abstract: BackgroundSubjects with non-O ABO blood group alleles have increased risk of pancreatic cancer. Glycosyltransferase activity is greater for the A(1) versus A(2) variant, whereas O01 and O02 variants are nonfunctioning. We hypothesized: 1) A(1) allele would confer greater risk than A(2) allele, 2) protective effect of the O allele would be equivalent for O01 and O02 variants, 3) secretor phenotype would modify the association with risk.MethodsWe determined ABO variants and secretor phenotype from single nucleotide polymorphisms in ABO and FUT2 genes in 1,533 cases and 1,582 controls from 12 prospective cohort studies. Adjusted odds ratios (OR) for pancreatic cancer were calculated using logistic regression.ResultsAn increased risk was observed in participants with A(1) but not A(2) alleles. Compared with subjects with genotype O/O, genotypes A(2)/O, A(2)/A(1), A(1)/O, and A(1)/A(1) had ORs of 0.96 (95% CI, 0.72-1.26), 1.46 (95% CI, 0.98-2.17), 1.48 (95% CI, 1.23-1.78), and 1.71 (95% CI, 1.18-2.47). Risk was similar for O01 and O02 variant O alleles. Compared with O01/O01, the ORs for each additional allele of O02, A(1), and A(2) were 1.00 (95% CI, 0.87-1.14), 1.38 (95% CI, 1.20-1.58), and 0.96 (95% CI, 0.77-1.20); P, O01 versus O02 = 0.94, A(1) versus A(2) = 0.004. Secretor phenotype was not an effect modifier (P-interaction = 0.63).ConclusionsAmong participants in a large prospective cohort consortium, ABO allele subtypes corresponding to increased glycosyltransferase activity were associated with increased pancreatic cancer risk.ImpactThese data support the hypothesis that ABO glycosyltransferase activity influences pancreatic cancer risk rather than actions of other nearby genes on chromosome 9q34.
Published: 2010

36. Family history of cancer and risk of pancreatic cancer: a pooled analysis from the Pancreatic Cancer Cohort Consortium (PanScan).

Author: Jacobs, Eric J, Chanock, Stephen J, Fuchs, Charles S, Lacroix, Andrea, McWilliams, Robert R, Steplowski, Emily, Stolzenberg-Solomon, Rachael Z, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Petersen, Gloria, Zheng, Wei, Agalliu, Ilir, Allen, Naomi E, Amundadottir, Laufey, Boutron-Ruault, Marie-Christine, Buring, Julie E, Canzian, Federico, Clipp, Sandra, Dorronsoro, Miren, Gaziano, J Michael, Giovannucci, Edward L, Hankinson, Susan E, Hartge, Patricia, Hoover, Robert N, Hunter, David J, Jacobs, Kevin B, Jenab, Mazda, Kraft, Peter, Kooperberg, Charles, Lynch, Shannon M, Sund, Malin, Mendelsohn, Julie B, Mouw, Tracy, Newton, Christina C, Overvad, Kim, Palli, Domenico, Peeters, Petra HM, Rajkovic, Aleksandar, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Kai, and Zeleniuch-Jacquotte, Anne
Subjects: Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Genome-Wide Association Study, Colo-Rectal Cancer, Clinical Research, Rare Diseases, Aging, Cancer, Digestive Diseases, Prostate Cancer, Ovarian Cancer, Pancreatic Cancer, Breast Cancer, Prevention, Urologic Diseases, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract: A family history of pancreatic cancer has consistently been associated with increased risk of pancreatic cancer. However, uncertainty remains about the strength of this association. Results from previous studies suggest a family history of select cancers (i.e., ovarian, breast and colorectal) could also be associated, although not as strongly, with increased risk of pancreatic cancer. We examined the association between a family history of 5 types of cancer (pancreas, prostate, ovarian, breast and colorectal) and risk of pancreatic cancer using data from a collaborative nested case-control study conducted by the Pancreatic Cancer Cohort Consortium. Cases and controls were from cohort studies from the United States, Europe and China, and a case-control study from the Mayo Clinic. Analyses of family history of pancreatic cancer included 1,183 cases and 1,205 controls. A family history of pancreatic cancer in a parent, sibling or child was associated with increased risk of pancreatic cancer [multivariate-adjusted odds ratios (ORs) = 1.76, 95% confidence interval (CI) = 1.19-2.61]. A family history of prostate cancer was also associated with increased risk (OR = 1.45, 95% CI = 1.12-1.89). There were no statistically significant associations with a family history of ovarian cancer (OR = 0.82, 95% CI = 0.52-1.31), breast cancer (OR = 1.21, 95% CI = 0.97-1.51) or colorectal cancer (OR = 1.17, 95% CI = 0.93-1.47). Our results confirm a moderate sized association between a family history of pancreatic cancer and risk of pancreatic cancer and also provide evidence for an association with a family history of prostate cancer worth further study.
Published: 2010

37. Alcohol intake and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium (PanScan)

Author: Michaud, Dominique S, Vrieling, Alina, Jiao, Li, Mendelsohn, Julie B, Steplowski, Emily, Lynch, Shannon M, Wactawski-Wende, Jean, Arslan, Alan A, Bas Bueno-de-Mesquita, H, Fuchs, Charles S, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Petersen, Gloria, Zheng, Wei, Allen, Naomi, Ammundadottir, Laufey, Bergmann, Manuela M, Boffetta, Paolo, Buring, Julie E, Canzian, Federico, Chanock, Stephen J, Clavel-Chapelon, Françoise, Clipp, Sandra, Freiberg, Matthew S, Michael Gaziano, J, Giovannucci, Edward L, Hankinson, Susan, Hartge, Patricia, Hoover, Robert N, Allan Hubbell, F, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin, Kooperberg, Charles, Kraft, Peter, Manjer, Jonas, Navarro, Carmen, Peeters, Petra HM, Shu, Xiao-Ou, Stevens, Victoria, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Tumino, Rosario, Vineis, Paolo, Virtamo, Jarmo, Wallace, Robert, Wolpin, Brian M, Yu, Kai, Zeleniuch-Jacquotte, Anne, and Stolzenberg-Solomon, Rachael Z
Subjects: Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Alcoholism, Alcohol Use and Health, Cancer, Digestive Diseases, Pancreatic Cancer, Rare Diseases, Clinical Research, Substance Misuse, Oral and gastrointestinal, Good Health and Well Being, Aged, Alcohol Drinking, Case-Control Studies, Cohort Studies, Female, Humans, Male, Pancreatic Neoplasms, Prospective Studies, Alcohol, Pancreatic cancer, Pooled analysis, Oncology and Carcinogenesis, Public Health and Health Services, Epidemiology, Oncology and carcinogenesis
Abstract: The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. >0 to
Published: 2010

38. Anthropometric Measures, Body Mass Index, and Pancreatic Cancer: A Pooled Analysis From the Pancreatic Cancer Cohort Consortium (PanScan)

Author: Arslan, Alan A, Helzlsouer, Kathy J, Kooperberg, Charles, Shu, Xiao-Ou, Steplowski, Emily, Bueno-de-Mesquita, H Bas, Fuchs, Charles S, Gross, Myron D, Jacobs, Eric J, Lacroix, Andrea Z, Petersen, Gloria M, Stolzenberg-Solomon, Rachael Z, Zheng, Wei, Albanes, Demetrius, Amundadottir, Laufey, Bamlet, William R, Barricarte, Aurelio, Bingham, Sheila A, Boeing, Heiner, Boutron-Ruault, Marie-Christine, Buring, Julie E, Chanock, Stephen J, Clipp, Sandra, Gaziano, J Michael, Giovannucci, Edward L, Hankinson, Susan E, Hartge, Patricia, Hoover, Robert N, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin B, Kraft, Peter, Lynch, Shannon M, Manjer, Jonas, Manson, Joann E, McTiernan, Anne, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Palli, Domenico, Rohan, Thomas E, Slimani, Nadia, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Virtamo, Jarmo, Wolpin, Brian M, Yu, Kai, Zeleniuch-Jacquotte, Anne, and Patel, Alpa V
Subjects: Obesity, Cancer, Clinical Research, Nutrition, Prevention, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Adult, Aged, Aged, 80 and over, Body Mass Index, Case-Control Studies, Female, Humans, Logistic Models, Male, Middle Aged, Overweight, Pancreatic Neoplasms, Risk Factors, Sex Distribution, United States, Waist Circumference, Pancreatic Cancer Cohort Consortium, Clinical Sciences, Opthalmology and Optometry, Public Health and Health Services
Abstract: BackgroundObesity has been proposed as a risk factor for pancreatic cancer.MethodsPooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, or = 35.0). Models were adjusted for potential confounders.ResultsIn all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; P(trend) < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; P(trend) < .03), and in women it was 1.34 (95% CI, 1.05-1.70; P(trend) = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; P(trend) = .003) but less so in men.ConclusionsThese findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.
Published: 2010

39. A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.

Author: Petersen, Gloria M, Amundadottir, Laufey, Fuchs, Charles S, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Jacobs, Kevin B, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gallinger, Steven, Gross, Myron, Helzlsouer, Kathy, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, LaCroix, Andrea, Li, Donghui, Mandelson, Margaret T, Olson, Sara H, Risch, Harvey A, Zheng, Wei, Albanes, Demetrius, Bamlet, William R, Berg, Christine D, Boutron-Ruault, Marie-Christine, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Howard, Barbara, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Kaaks, Rudolf, Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C, Lynch, Shannon M, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Parikh, Hemang, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Rodriguez, Laudina, Seminara, Daniela, Shu, Xiao-Ou, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wang, Zhaoming, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Fraumeni, Joseph F, Hoover, Robert N, Hartge, Patricia, and Chanock, Stephen J
Subjects: Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 13, Humans, Carcinoma, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Loci, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract: We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.
Published: 2010

40. Pancreatic cancer risk and ABO blood group alleles: results from the pancreatic cancer cohort consortium.

Author: Wolpin, Brian M, Kraft, Peter, Gross, Myron, Helzlsouer, Kathy, Bueno-de-Mesquita, H Bas, Steplowski, Emily, Stolzenberg-Solomon, Rachael Z, Arslan, Alan A, Jacobs, Eric J, Lacroix, Andrea, Petersen, Gloria, Zheng, Wei, Albanes, Demetrius, Allen, Naomi E, Amundadottir, Laufey, Anderson, Garnet, Boutron-Ruault, Marie-Christine, Buring, Julie E, Canzian, Federico, Chanock, Stephen J, Clipp, Sandra, Gaziano, John Michael, Giovannucci, Edward L, Hallmans, Göran, Hankinson, Susan E, Hoover, Robert N, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin, Kooperberg, Charles, Lynch, Shannon M, Mendelsohn, Julie B, Michaud, Dominique S, Overvad, Kim, Patel, Alpa V, Rajkovic, Aleksandar, Sanchéz, Maria-José, Shu, Xiao-Ou, Slimani, Nadia, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Vineis, Paolo, Virtamo, Jarmo, Wactawski-Wende, Jean, Yu, Kai, Zeleniuch-Jacquotte, Anne, Hartge, Patricia, and Fuchs, Charles S
Subjects: Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, ABO Blood-Group System, Logistic Models, Odds Ratio, Risk Factors, Cohort Studies, Gene Frequency, Genotype, Alleles, Aged, Middle Aged, Female, Male, Clinical Research, Genetics, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Cancer, Prevention, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract: A recent genome-wide association study (PanScan) identified significant associations at the ABO gene locus with risk of pancreatic cancer, but the influence of specific ABO genotypes remains unknown. We determined ABO genotypes (OO, AO, AA, AB, BO, and BB) in 1,534 cases and 1,583 controls from 12 prospective cohorts in PanScan, grouping participants by genotype-derived serologic blood type (O, A, AB, and B). Adjusted odds ratios (ORs) for pancreatic cancer by ABO alleles were calculated using logistic regression. Compared with blood type O, the ORs for pancreatic cancer in subjects with types A, AB, and B were 1.38 [95% confidence interval (95% CI), 1.18-1.62], 1.47 (95% CI, 1.07-2.02), and 1.53 (95% CI, 1.21-1.92), respectively. The incidence rates for blood types O, A, AB, and B were 28.9, 39.9, 41.8, and 44.5 cases per 100,000 subjects per year. An increase in risk was noted with the addition of each non-O allele. Compared with OO genotype, subjects with AO and AA genotype had ORs of 1.33 (95% CI, 1.13-1.58) and 1.61 (95% CI, 1.22-2.18), whereas subjects with BO and BB genotypes had ORs of 1.45 (95% CI, 1.14-1.85) and 2.42 (1.28-4.57). The population attributable fraction for non-O blood type was 19.5%. In a joint model with smoking, current smokers with non-O blood type had an adjusted OR of 2.68 (95% CI, 2.03-3.54) compared with nonsmokers of blood type O. We concluded that ABO genotypes were significantly associated with pancreatic cancer risk.
Published: 2010

41. Obesity and Cancer Risk among White and Black United States Veterans

Author: Samanic, Claudine, Gridley, Gloria, Chow, Wong-Ho, Lubin, Jay, Hoover, Robert N., and Fraumeni,, Joseph F.
Published: 2004

42. Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer.

Author: Amundadottir, Laufey, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Fuchs, Charles S, Petersen, Gloria M, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Zheng, Wei, Albanes, Demetrius, Bamlet, William, Berg, Christine D, Berrino, Franco, Bingham, Sheila, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clavel-Chapelon, Françoise, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Fox, John W, Gallinger, Steven, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, González, Carlos A, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Holly, Elizabeth A, Hunter, David J, Hutchinson, Amy, Jackson, Rebecca, Jacobs, Kevin B, Jenab, Mazda, Kaaks, Rudolf, Klein, Alison P, Kooperberg, Charles, Kurtz, Robert C, Li, Donghui, Lynch, Shannon M, Mandelson, Margaret, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Olson, Sara H, Overvad, Kim, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Risch, Harvey A, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Chanock, Stephen J, Hartge, Patricia, and Hoover, Robert N
Subjects: Chromosomes, Human, Pair 9, Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, ABO Blood-Group System, Logistic Models, Odds Ratio, Risk Factors, Case-Control Studies, Cohort Studies, Prospective Studies, Gene Frequency, Genotype, Haplotypes, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Alleles, Introns, United States, Female, Male, Genetic Variation, Genome-Wide Association Study, Prevention, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract: We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.
Published: 2009

43. Cigarette Smoking and Pancreatic Cancer: A Pooled Analysis From the Pancreatic Cancer Cohort Consortium

Author: Lynch, Shannon M, Vrieling, Alina, Lubin, Jay H, Kraft, Peter, Mendelsohn, Julie B, Hartge, Patricia, Canzian, Federico, Steplowski, Emily, Arslan, Alan A, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Petersen, Gloria, Zheng, Wei, Albanes, Demetrius, Amundadottir, Laufey, Bingham, Sheila A, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Chanock, Stephen J, Clipp, Sandra, Hoover, Robert N, Jacobs, Kevin, Johnson, Karen C, Kooperberg, Charles, Luo, Juhua, Messina, Catherine, Palli, Domenico, Patel, Alpa V, Riboli, Elio, Shu, Xiao-Ou, Rodriguez Suarez, Laudina, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Tong, Elissa, Trichopoulos, Dimitrios, Virtamo, Jarmo, Ye, Weimin, Yu, Kai, Zeleniuch-Jacquette, Anne, Bueno-de-Mesquita, H Bas, and Stolzenberg-Solomon, Rachael Z
Subjects: Tobacco, Digestive Diseases, Cancer, Pancreatic Cancer, Rare Diseases, Prevention, Tobacco Smoke and Health, Prevention of disease and conditions, and promotion of well-being, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Female, Humans, Male, Middle Aged, Pancreatic Neoplasms, Prospective Studies, Risk, Smoking, Smoking Cessation, United States, pancreas, pancreatic neoplasms, smoking, tobacco use cessation, Mathematical Sciences, Medical and Health Sciences, Epidemiology
Abstract: Smoking is an established risk factor for pancreatic cancer; however, detailed examination of the association of smoking intensity, smoking duration, and cumulative smoking dose with pancreatic cancer is limited. The authors analyzed pooled data from the international Pancreatic Cancer Cohort Consortium nested case-control study (1,481 cases, 1,539 controls). Odds ratios and 95% confidence intervals were calculated by using unconditional logistic regression. Smoking intensity effects were examined with an excess odds ratio model that was linear in pack-years and exponential in cigarettes smoked per day and its square. When compared with never smokers, current smokers had a significantly elevated risk (odds ratio (OR) = 1.77, 95% confidence interval (CI): 1.38, 2.26). Risk increased significantly with greater intensity (> or =30 cigarettes/day: OR = 1.75, 95% CI: 1.27, 2.42), duration (> or =50 years: OR = 2.13, 95% CI: 1.25, 3.62), and cumulative smoking dose (> or =40 pack-years: OR = 1.78, 95% CI: 1.35, 2.34). Risk more than 15 years after smoking cessation was similar to that for never smokers. Estimates of excess odds ratio per pack-year declined with increasing intensity, suggesting greater risk for total exposure delivered at lower intensity for longer duration than for higher intensity for shorter duration. This finding and the decline in risk after smoking cessation suggest that smoking has a late-stage effect on pancreatic carcinogenesis.
Published: 2009

44. Population-Density and County-Level Variation in Breast Cancer Mortality Rates among White Women Residing in the Northeastern and Southern United States

Author: Sturgeon, Susan R., Graubard, Barry I., Schairer, Catherine, McAdams, Mary, Hoover, Robert N., and Gail, Mitchell H.
Published: 2003

45. Associations of Maternal and Umbilical Cord Hormone Concentrations with Maternal, Gestational and Neonatal Factors (United States)

Author: Troisi, Rebecca, Potischman, Nancy, Roberts, James, Siiteri, Pentti, Daftary, Ashi, Sims, Cynthia, and Hoover, Robert N.
Published: 2003

46. Why Do Black Americans Have a Higher Risk of Pancreatic Cancer Than White Americans?

Author: Silverman, Debra T., Hoover, Robert N., Brown, Linda M., Swanson, G. Marie, Schiffman, Mark, Greenberg, Raymond S., Hayes, Richard B., Lillemoe, Keith D., Schoenberg, Janet B., Schwartz, Ann G., Liff, Jonathan, Pottern, Linda M., and Fraumeni,, Joseph F.
Published: 2003

47. Risk of Breast Cancer in Women Exposed to Diethylstilbestrol in Utero: Preliminary Results (United States)

Author: Palmer, Julie R., Hatch, Elizabeth E., Rosenberg, Carol L., Hartge, Patricia, Kaufman, Raymond H., Titus-Ernstoff, Linda, Noller, Kenneth L., Herbst, Arthur L., Rao, R. Sowmya, Troisi, Rebecca, Colton, Theodore, and Hoover, Robert N.
Published: 2002

48. Mortality among Augmentation Mammoplasty Patients

Author: Brinton, Louise A., Lubin, Jay H., Burich, Mary Cay, Colton, Theodore, and Hoover, Robert N.
Published: 2001

49. Breast Cancer Following Augmentation Mammoplasty (United States)

Author: Brinton, Louise A., Lubin, Jay H., Burich, Mary Cay, Colton, Theodore, Brown, S. Lori, and Hoover, Robert N.
Published: 2000

50. Measurement Error Does Not Explain the Persistence of a Body Mass Index Association with Endometrial Cancer after Adjustment for Endogenous Hormones

Author: Potischman, Nancy, Gail, Mitchell H., Troisi, Rebecca, Wacholder, Sholom, and Hoover, Robert N.
Published: 1999

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