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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, Saunders, Edward, Chen, Fei, Janivara, Rohini, Darst, Burcu, Sheng, Xin, Xu, Yili, Chou, Alisha, Benlloch, Sara, Dadaev, Tokhir, Brook, Mark, Plym, Anna, Sahimi, Ali, Hoffman, Thomas, 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, Schleutker, Johanna, Tammela, Teuvo, Sipeky, Csilla, Auvinen, Anssi, Giles, Graham, Southey, Melissa, MacInnis, Robert, Cybulski, Cezary, Wokolorczyk, Dominika, Lubinski, Jan, Rentsch, Christopher, Cho, Kelly, Mcmahon, Benjamin, Neal, David, Donovan, Jenny, Hamdy, Freddie, Martin, Richard, Nordestgaard, Borge, Nielsen, Sune, Weischer, Maren, Bojesen, Stig, Røder, Andreas, Stroomberg, Hein, Batra, Jyotsna, Chambers, Suzanne, Horvath, Lisa, Clements, Judith, Tilly, Wayne, Risbridger, Gail, Gronberg, Henrik, Aly, Markus, Szulkin, Robert, Eklund, Martin, Nordstrom, Tobias, Pashayan, Nora, Dunning, Alison, Ghoussaini, Maya, Travis, Ruth, Key, Tim, Riboli, Elio, Park, Jong, Sellers, Thomas, Lin, Hui-Yi, Albanes, Demetrius, Weinstein, Stephanie, Cook, Michael, Mucci, Lorelei, Giovannucci, Edward, Lindstrom, Sara, Kraft, Peter, Hunter, David, Penney, Kathryn, Turman, Constance, Tangen, Catherine, Goodman, Phyllis, Thompson, Ian, Hamilton, Robert, Fleshner, Neil, Finelli, Antonio, Parent, Marie-Élise, Stanford, Janet, Ostrander, Elaine, Koutros, Stella, Beane Freeman, Laura, Stampfer, Meir, Wolk, Alicja, and Håkansson, Niclas

Subjects
Humans, Male, Black People, Genetic Predisposition to Disease, Genome-Wide Association Study, Hispanic or Latino, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Risk Factors, White People, Asian People
Abstract

The transferability and clinical value of genetic risk scores (GRSs) across populations remain limited due to an imbalance in genetic studies across ancestrally diverse populations. Here we conducted a multi-ancestry genome-wide association study of 156,319 prostate cancer cases and 788,443 controls of European, African, Asian and Hispanic men, reflecting a 57% increase in the number of non-European cases over previous prostate cancer genome-wide association studies. We identified 187 novel risk variants for prostate cancer, increasing the total number of risk variants to 451. An externally replicated multi-ancestry GRS was associated with risk that ranged from 1.8 (per standard deviation) in African ancestry men to 2.2 in European ancestry men. The GRS was associated with a greater risk of aggressive versus non-aggressive disease in men of African ancestry (P = 0.03). Our study presents novel prostate cancer susceptibility loci and a GRS with effective risk stratification across ancestry groups.

Published
2023

2. Two Novel Susceptibility Loci for Prostate Cancer in Men of African Ancestry

Author

Conti, David V, Wang, Kan, Sheng, Xin, Bensen, Jeannette T, Hazelett, Dennis J, Cook, Michael B, Ingles, Sue A, Kittles, Rick A, Strom, Sara S, Rybicki, Benjamin A, Nemesure, Barbara, Isaacs, William B, Stanford, Janet L, Zheng, Wei, Sanderson, Maureen, John, Esther M, Park, Jong Y, Xu, Jianfeng, Stevens, Victoria L, Berndt, Sonja I, Huff, Chad D, Wang, Zhaoming, Yeboah, Edward D, Tettey, Yao, Biritwum, Richard B, Adjei, Andrew A, Tay, Evelyn, Truelove, Ann, Niwa, Shelley, Sellers, Thomas A, Yamoah, Kosj, Murphy, Adam B, Crawford, Dana C, Gapstur, Susan M, Bush, William S, Aldrich, Melinda C, Cussenot, Olivier, Petrovics, Gyorgy, Cullen, Jennifer, Neslund-Dudas, Christine, Stern, Mariana C, Jarai, Zsofia-Kote, Govindasami, Koveela, Chokkalingam, Anand P, Hsing, Ann W, Goodman, Phyllis J, Hoffmann, Thomas, Drake, Bettina F, Hu, Jennifer J, Clark, Peter E, Van Den Eeden, Stephen K, Blanchet, Pascal, Fowke, Jay H, Casey, Graham, Hennis, Anselm JM, Han, Ying, Lubwama, Alexander, Thompson, Ian M, Leach, Robin, Easton, Douglas F, Schumacher, Fredrick, Van den Berg, David J, Gundell, Susan M, Stram, Alex, Wan, Peggy, Xia, Lucy, Pooler, Loreall C, Mohler, James L, Fontham, Elizabeth TH, Smith, Gary J, Taylor, Jack A, Srivastava, Shiv, Eeles, Rosalind A, Carpten, John, Kibel, Adam S, Multigner, Luc, Parent, Marie-Elise, Menegaux, Florence, Cancel-Tassin, Geraldine, Klein, Eric A, Brureau, Laurent, Stram, Daniel O, Watya, Stephen, Chanock, Stephen J, Witte, John S, Blot, William J, Henderson, Brian E, and Haiman, Christopher A

Subjects
Aging, Human Genome, Cancer, Prevention, Prostate Cancer, Biotechnology, Clinical Research, Genetics, Urologic Diseases, 2.1 Biological and endogenous factors, Aetiology, Blacks, Case-Control Studies, Checkpoint Kinase 2, Chromosomes, Human, Pair 13, Chromosomes, Human, Pair 22, Gene Frequency, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Insulin Receptor Substrate Proteins, Male, Polymorphism, Single Nucleotide, Prostatic Neoplasms, PRACTICAL/ELLIPSE Consortium, Black People, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Prostate cancer incidence is 1.6-fold higher in African Americans than in other populations. The risk factors that drive this disparity are unknown and potentially consist of social, environmental, and genetic influences. To investigate the genetic basis of prostate cancer in men of African ancestry, we performed a genome-wide association meta-analysis using two-sided statistical tests in 10 202 case subjects and 10 810 control subjects. We identified novel signals on chromosomes 13q34 and 22q12, with the risk-associated alleles found only in men of African ancestry (13q34: rs75823044, risk allele frequency = 2.2%, odds ratio [OR] = 1.55, 95% confidence interval [CI] = 1.37 to 1.76, P = 6.10 × 10-12; 22q12.1: rs78554043, risk allele frequency = 1.5%, OR = 1.62, 95% CI = 1.39 to 1.89, P = 7.50 × 10-10). At 13q34, the signal is located 5' of the gene IRS2 and 3' of a long noncoding RNA, while at 22q12 the candidate functional allele is a missense variant in the CHEK2 gene. These findings provide further support for the role of ancestry-specific germline variation in contributing to population differences in prostate cancer risk.

Published
2017

3. Polygenic Risk Score Modifies Prostate Cancer Risk of Pathogenic Variants in Men of African Ancestry

Author

Hughley, Raymond W., primary, Matejcic, Marco, additional, Song, Ziwei, additional, Sheng, Xin, additional, Wan, Peggy, additional, Xia, Lucy, additional, Hart, Steven N., additional, Hu, Chunling, additional, Yadav, Siddhartha, additional, Lubwama, Alexander, additional, Kiddu, Vicky, additional, Asiimwe, Frank, additional, Amanya, Colline, additional, Mutema, George, additional, Job, Kuteesa, additional, Ssebakumba, Mbaaga Kigongo, additional, Ingles, Sue Ann, additional, Hamilton, Ann S, additional, Couch, Fergus J, additional, Watya, Stephen, additional, Conti, David V., additional, Darst, Burcu F, additional, and Haiman, Christopher A, additional

Published
2023
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5. Evaluating approaches for constructing polygenic risk scores for prostate cancer in men of African and European ancestry

Author

Darst, Burcu F., primary, Shen, Jiayi, additional, Madduri, Ravi K., additional, Rodriguez, Alexis A., additional, Xiao, Yukai, additional, Sheng, Xin, additional, Saunders, Edward J., additional, Dadaev, Tokhir, additional, Brook, Mark N., additional, Hoffmann, Thomas J., additional, Muir, Kenneth, additional, Wan, Peggy, additional, Le Marchand, Loic, additional, Wilkens, Lynne, additional, Wang, Ying, additional, Schleutker, Johanna, additional, MacInnis, Robert J., additional, Cybulski, Cezary, additional, Neal, David E., additional, Nordestgaard, Børge G., additional, Nielsen, Sune F., additional, Batra, Jyotsna, additional, Clements, Judith A., additional, Cancer BioResource, Australian Prostate, additional, Grönberg, Henrik, additional, Pashayan, Nora, additional, Travis, Ruth C., additional, Park, Jong Y., additional, Albanes, Demetrius, additional, Weinstein, Stephanie, additional, Mucci, Lorelei A., additional, Hunter, David J., additional, Penney, Kathryn L., additional, Tangen, Catherine M., additional, Hamilton, Robert J., additional, Parent, Marie-Élise, additional, Stanford, Janet L., additional, Koutros, Stella, additional, Wolk, Alicja, additional, Sørensen, Karina D., additional, Blot, William J., additional, Yeboah, Edward D., additional, Mensah, James E., additional, Lu, Yong-Jie, additional, Schaid, Daniel J., additional, Thibodeau, Stephen N., additional, West, Catharine M., additional, Maier, Christiane, additional, Kibel, Adam S., additional, Cancel-Tassin, Géraldine, additional, Menegaux, Florence, additional, John, Esther M., additional, Grindedal, Eli Marie, additional, Khaw, Kay-Tee, additional, Ingles, Sue A., additional, Vega, Ana, additional, Rosenstein, Barry S., additional, Teixeira, Manuel R., additional, Kogevinas, Manolis, additional, Cannon-Albright, Lisa, additional, Huff, Chad, additional, Multigner, Luc, additional, Kaneva, Radka, additional, Leach, Robin J., additional, Brenner, Hermann, additional, Hsing, Ann W., additional, Kittles, Rick A., additional, Murphy, Adam B., additional, Logothetis, Christopher J., additional, Neuhausen, Susan L., additional, Isaacs, William B., additional, Nemesure, Barbara, additional, Hennis, Anselm J., additional, Carpten, John, additional, Pandha, Hardev, additional, De Ruyck, Kim, additional, Xu, Jianfeng, additional, Razack, Azad, additional, Teo, Soo-Hwang, additional, Newcomb, Lisa F., additional, Fowke, Jay H., additional, Neslund-Dudas, Christine, additional, Rybicki, Benjamin A., additional, Gamulin, Marija, additional, Usmani, Nawaid, additional, Claessens, Frank, additional, Gago-Dominguez, Manuela, additional, Castelao, Jose Esteban, additional, Townsend, Paul A., additional, Crawford, Dana C., additional, Petrovics, Gyorgy, additional, Casey, Graham, additional, Roobol, Monique J., additional, Hu, Jennifer F., additional, Berndt, Sonja I., additional, Van Den Eeden, Stephen K., additional, Easton, Douglas F., additional, Chanock, Stephen J., additional, Cook, Michael B., additional, Wiklund, Fredrik, additional, Witte, John S., additional, Eeles, Rosalind A., additional, Kote-Jarai, Zsofia, additional, Watya, Stephen, additional, Gaziano, John M., additional, Justice, Amy C., additional, Conti, David V., additional, and Haiman, Christopher A., additional

Published
2023
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6. Genetic variants associated with fasting glucose and insulin concentrations in an ethnically diverse population: results from the Population Architecture using Genomics and Epidemiology (PAGE) study

Author

Fesinmeyer, Megan D, Meigs, James B, North, Kari E, Schumacher, Fredrick R, Bůžková, Petra, Franceschini, Nora, Haessler, Jeffrey, Goodloe, Robert, Spencer, Kylee L, Voruganti, Venkata, Howard, Barbara V, Jackson, Rebecca, Kolonel, Laurence N, Liu, Simin, Manson, JoAnn E, Monroe, Kristine R, Mukamal, Kenneth, Dilks, Holli H, Pendergrass, Sarah A, Nato, Andrew, Wan, Peggy, Wilkens, Lynne R, Marchand, Loic, Ambite, José, Buyske, Steven, Florez, Jose C, Crawford, Dana C, Hindorff, Lucia A, Haiman, Christopher A, Peters, Ulrike, and Pankow, James S

Abstract

Abstract Background Multiple genome-wide association studies (GWAS) within European populations have implicated common genetic variants associated with insulin and glucose concentrations. In contrast, few studies have been conducted within minority groups, which carry the highest burden of impaired glucose homeostasis and type 2 diabetes in the U.S. Methods As part of the 'Population Architecture using Genomics and Epidemiology (PAGE) Consortium, we investigated the association of up to 10 GWAS-identified single nucleotide polymorphisms (SNPs) in 8 genetic regions with glucose or insulin concentrations in up to 36,579 non-diabetic subjects including 23,323 European Americans (EA) and 7,526 African Americans (AA), 3,140 Hispanics, 1,779 American Indians (AI), and 811 Asians. We estimated the association between each SNP and fasting glucose or log-transformed fasting insulin, followed by meta-analysis to combine results across PAGE sites. Results Overall, our results show that 9/9 GWAS SNPs are associated with glucose in EA (p = 0.04 to 9 × 10-15), versus 3/9 in AA (p= 0.03 to 6 × 10-5), 3/4 SNPs in Hispanics, 2/4 SNPs in AI, and 1/2 SNPs in Asians. For insulin we observed a significant association with rs780094/GCKR in EA, Hispanics and AI only. Conclusions Generalization of results across multiple racial/ethnic groups helps confirm the relevance of some of these loci for glucose and insulin metabolism. Lack of association in non-EA groups may be due to insufficient power, or to unique patterns of linkage disequilibrium.

Published
2013

7. Genome-wide association study of prostate cancer in men of African ancestry identifies a susceptibility locus at 17q21

Author

Haiman, Christopher A, Chen, Gary K, Blot, William J, Strom, Sara S, Berndt, Sonja I, Kittles, Rick A, Rybicki, Benjamin A, Isaacs, William B, Ingles, Sue A, Stanford, Janet L, Diver, W Ryan, Witte, John S, Hsing, Ann W, Nemesure, Barbara, Rebbeck, Timothy R, Cooney, Kathleen A, Xu, Jianfeng, Kibel, Adam S, Hu, Jennifer J, John, Esther M, Gueye, Serigne M, Watya, Stephen, Signorello, Lisa B, Hayes, Richard B, Wang, Zhaoming, Yeboah, Edward, Tettey, Yao, Cai, Qiuyin, Kolb, Suzanne, Ostrander, Elaine A, Zeigler-Johnson, Charnita, Yamamura, Yuko, Neslund-Dudas, Christine, Haslag-Minoff, Jennifer, Wu, William, Thomas, Venetta, Allen, Glenn O, Murphy, Adam, Chang, Bao-Li, Zheng, S Lilly, Leske, M Cristina, Wu, Suh-Yuh, Ray, Anna M, Hennis, Anselm JM, Thun, Michael J, Carpten, John, Casey, Graham, Carter, Erin N, Duarte, Edder R, Xia, Lucy Y, Sheng, Xin, Wan, Peggy, Pooler, Loreall C, Cheng, Iona, Monroe, Kristine R, Schumacher, Fredrick, Le Marchand, Loic, Kolonel, Laurence N, Chanock, Stephen J, Berg, David Van Den, Stram, Daniel O, and Henderson, Brian E

Subjects
Biological Sciences, Genetics, Human Genome, Aging, Urologic Diseases, Prevention, Prostate Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Black or African American, Chromosomes, Human, Pair 17, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide, Prostatic Neoplasms, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

In search of common risk alleles for prostate cancer that could contribute to high rates of the disease in men of African ancestry, we conducted a genome-wide association study, with 1,047,986 SNP markers examined in 3,425 African-Americans with prostate cancer (cases) and 3,290 African-American male controls. We followed up the most significant 17 new associations from stage 1 in 1,844 cases and 3,269 controls of African ancestry. We identified a new risk variant on chromosome 17q21 (rs7210100, odds ratio per allele = 1.51, P = 3.4 × 10(-13)). The frequency of the risk allele is ∼5% in men of African descent, whereas it is rare in other populations (

Published
2011

10. Evaluating Approaches for Constructing Polygenic Risk Scores for Prostate Cancer in Men of African and European Ancestry

Author

Darst, Burcu F., Shen, Jiayi, Madduri, Ravi K., Rodriguez, Alexis A., Xiao, Yukai, Sheng, Xin, Saunders, Edward J., Dadaev, Tokhir, Brook, Mark N., Hoffmann, Thomas J., Muir, Kenneth, Wan, Peggy, Marchand, Loic Le, Wilkens, Lynne, Wang, Ying, Schleutker, Johanna, MacInnis, Robert J., Cybulski, Cezary, Neal, David E., G. Nordestgaard, Børge, Nielsen, Sune F., Batra, Jyotsna, Clements, Judith A., Grönberg, Henrik, Pashayan, Nora, Travis, Ruth C., Park, Jong Y., Albanes, Demetrius, Weinstein, Stephanie, Mucci, Lorelei A., Hunter, David J., Penney, Kathryn L., Tangen, Catherine M., Hamilton, Robert J., Parent, Marie-Élise, Stanford, Janet L., Koutros, Stella, Wolk, Alicja, Sørensen, Karina D., Blot, William J., Yeboah, Edward D., Mensah, James E., Lu, Yong-Jie, Schaid, Daniel J., Thibodeau, Stephen N., West, Catharine M., Maier, Christiane, Kibel, Adam S., Cancel-Tassin, Géraldine, Menegaux, Florence, John, Esther M., Grindedal, Eli Marie, Khaw, Kay-Tee, Ingles, Sue A., Vega, Ana, Rosenstein, Barry S., Teixeira, Manuel R., Kogevinas, Manolis, Cannon-Albright, Lisa, Huff, Chad, Multigner, Luc, Kaneva, Radka, Leach, Robin J., Brenner, Hermann, Hsing, Ann W., Kittles, Rick A., Murphy, Adam B., Logothetis, Christopher J., Neuhausen, Susan L., Isaacs, William B., Nemesure, Barbara, Hennis, Anselm J., Carpten, John, Pandha, Hardev, De Ruyck, Kim, Xu, Jianfeng, Razack, Azad, Teo, Soo-Hwang, Newcomb, Lisa F., Fowke, Jay H., Neslund-Dudas, Christine, Rybicki, Benjamin A., Gamulin, Marija, Usmani, Nawaid, Claessens, Frank, Gago-Dominguez, Manuela, Castelao, Jose Esteban, Townsend, Paul A., Crawford, Dana C., Petrovics, Gyorgy, Casey, Graham, Roobol, Monique J., Hu, Jennifer F., Berndt, Sonja I., Van Den Eeden, Stephen K., Easton, Douglas F., Chanock, Stephen J., Cook, Michael B., Wiklund, Fredrik, Witte, John S., Eeles, Rosalind A., Kote-Jarai, Zsofia, Watya, Stephen, Gaziano, John M., Justice, Amy C., Conti, David V., and Haiman, Christopher A.

Subjects
Article
Abstract

Genome-wide polygenic risk scores (GW-PRS) have been reported to have better predictive ability than PRS based on genome-wide significance thresholds across numerous traits. We compared the predictive ability of several GW-PRS approaches to a recently developed PRS of 269 established prostate cancer risk variants from multi-ancestry GWAS and fine-mapping studies (PRS (269) ). GW-PRS models were trained using a large and diverse prostate cancer GWAS of 107,247 cases and 127,006 controls used to develop the multi-ancestry PRS (269) . Resulting models were independently tested in 1,586 cases and 1,047 controls of African ancestry from the California/Uganda Study and 8,046 cases and 191,825 controls of European ancestry from the UK Biobank and further validated in 13,643 cases and 210,214 controls of European ancestry and 6,353 cases and 53,362 controls of African ancestry from the Million Veteran Program. In the testing data, the best performing GW-PRS approach had AUCs of 0.656 (95% CI=0.635-0.677) in African and 0.844 (95% CI=0.840-0.848) in European ancestry men and corresponding prostate cancer OR of 1.83 (95% CI=1.67-2.00) and 2.19 (95% CI=2.14-2.25), respectively, for each SD unit increase in the GW-PRS. However, compared to the GW-PRS, in African and European ancestry men, the PRS (269) had larger or similar AUCs (AUC=0.679, 95% CI=0.659-0.700 and AUC=0.845, 95% CI=0.841-0.849, respectively) and comparable prostate cancer OR (OR=2.05, 95% CI=1.87-2.26 and OR=2.21, 95% CI=2.16-2.26, respectively). Findings were similar in the validation data. This investigation suggests that current GW-PRS approaches may not improve the ability to predict prostate cancer risk compared to the multi-ancestry PRS (269) constructed with fine-mapping.

Published
2023

13. Clonal hematopoiesis and risk of prostate cancer in large samples of European ancestry men

Author

Wang, Anqi, primary, Xu, Yili, additional, Yu, Yao, additional, Nead, Kevin T, additional, Kim, TaeBeom, additional, Xu, Keren, additional, Dadaev, Tokhir, additional, Saunders, Ed, additional, Sheng, Xin, additional, Wan, Peggy, additional, Pooler, Loreall, additional, Xia, Lucy Y, additional, Chanock, Stephen, additional, Berndt, Sonja I, additional, Gapstur, Susan M, additional, Stevens, Victoria, additional, Albanes, Demetrius, additional, Weinstein, Stephanie J, additional, Gnanapragasam, Vincent, additional, Giles, Graham G, additional, Nguyen-Dumont, Tu, additional, Milne, Roger L, additional, Pomerantz, Mark M, additional, Schmidt, Julie A, additional, Stopsack, Konrad H, additional, Mucci, Lorelei A, additional, Catalona, William J, additional, Hetrick, Kurt N, additional, Doheny, Kimberly F, additional, MacInnis, Robert J, additional, Southey, Melissa C, additional, Eeles, Rosalind A, additional, Wiklund, Fredrik, additional, Kote-Jarai, Zsofia, additional, de Smith, Adam J, additional, Conti, David V, additional, Huff, Chad, additional, Haiman, Christopher A, additional, and Darst, Burcu F, additional

Published
2022
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15. Abstract 688: Multi-stage exome sequencing study of 17,546 aggressive and non-aggressive prostate cancer cases

Author

Darst, Burcu F., primary, Saunders, Ed, additional, Dadaev, Tokhir, additional, Sheng, Xin, additional, Wan, Peggy, additional, Pooler, Loreall, additional, Xia, Lucy Y., additional, Chanock, Stephen, additional, Berndt, Sonja I., additional, Gapstur, Susan M., additional, Stevens, Victoria, additional, Albanes, Demetrius, additional, Weinstein, Stephanie J., additional, Gnanapragasam, Vincent, additional, Giles, Graham G., additional, Nguyen-Dumont, Tu, additional, Milne, Roger L., additional, Pomerantz, Mark M., additional, Schmidt, Julie A., additional, Travis, Ruth C., additional, Key, Timothy J., additional, Stopsack, Konrad H., additional, Mucci, Lorelei A., additional, Catalona, William J., additional, Marosy, Beth, additional, Hetrick, Kurt N., additional, Doheny, Kimberly F., additional, MacInnis, Robert J., additional, Southey, Melissa C., additional, Eeles, Rosalind A., additional, Wiklund, Fredrik, additional, Kote-Jarai, Zsofia, additional, Conti, David V., additional, and Haiman, Christopher A., additional

Published
2022
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18. Genome-wide association study of colorectal cancer in Hispanics

Author

Schmit, Stephanie L., Schumacher, Fredrick R., Edlund, Christopher K., Conti, David V., Ihenacho, Ugonna, Wan, Peggy, Van Den Berg, David, Casey, Graham, Fortini, Barbara K., Lenz, Heinz-Josef, Tusié-Luna, Teresa, Aguilar-Salinas, Carlos A., Moreno-Macías, Hortensia, Huerta-Chagoya, Alicia, Ordóñez-Sánchez, María Luisa, Rodríguez-Guillén, Rosario, Cruz-Bautista, Ivette, Rodríguez-Torres, Maribel, Muñóz-Hernández, Linda Liliana, Arellano-Campos, Olimpia, Gómez, Donají, Alvirde, Ulices, González-Villalpando, Clicerio, González-Villalpando, María Elena, Le Marchand, Loic, Haiman, Christopher A., and Figueiredo, Jane C.

Published
2016
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20. 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 LJ, 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, 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, and Lu, Yong-Jie

Subjects
Male, Urologic Diseases, Aging, Quantitative Trait Loci, Medical and Health Sciences, Risk Factors, Clinical Research, Odds Ratio, Genetics, Humans, 2.1 Biological and endogenous factors, Neoplasm Invasiveness, Genetic Predisposition to Disease, Aetiology, Cancer, Prevention, Prostate Cancer, Racial Groups, Human Genome, Prostatic Neoplasms, Molecular Sequence Annotation, Genomics, Middle Aged, Biological Sciences, Phenotype, Good Health and Well Being, Genetic Loci, Software, Genome-Wide Association Study, Statistical Distributions, Developmental Biology
Abstract

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.

Published
2021

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

Author

Chen, Fang, Chen, Gary K., Stram, Daniel O., Millikan, Robert C., Ambrosone, Christine B., John, Esther M., Bernstein, Leslie, Zheng, Wei, Palmer, Julie R., Hu, Jennifer J., Rebbeck, Tim R., Ziegler, Regina G., Nyante, Sarah, Bandera, Elisa V., Ingles, Sue A., Press, Michael F., Ruiz-Narvaez, Edward A., Deming, Sandra L., Rodriguez-Gil, Jorge L., DeMichele, Angela, Chanock, Stephen J., Blot, William, Signorello, Lisa, Cai, Qiuyin, Li, Guoliang, Long, Jirong, Huo, Dezheng, Zheng, Yonglan, Cox, Nancy J., Olopade, Olufunmilayo I., Ogundiran, Temidayo O., Adebamowo, Clement, Nathanson, Katherine L., Domchek, Susan M., Simon, Michael S., Hennis, Anselm, Nemesure, Barbara, Wu, Suh-Yuh, Leske, M. Cristina, Ambs, Stefan, Hutter, Carolyn M., Young, Alicia, Kooperberg, Charles, Peters, Ulrike, Rhie, Suhn K., Wan, Peggy, Sheng, Xin, Pooler, Loreall C., Van Den Berg, David J., Le Marchand, Loic, Kolonel, Laurence N., Henderson, Brian E., and Haiman, Christopher A.

Published
2013
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23. Consistent Directions of Effect for Established Type 2 Diabetes Risk Variants Across Populations: The Population Architecture using Genomics and Epidemiology (PAGE) Consortium

Author

Haiman, Christopher A., Fesinmeyer, Megan D., Spencer, Kylee L., Bůžková, Petra, Voruganti, V. Saroja, Wan, Peggy, Haessler, Jeff, Franceschini, Nora, Monroe, Kristine R., Howard, Barbara V., Jackson, Rebecca D., Florez, Jose C., Kolonel, Laurence N., Buyske, Steven, Goodloe, Robert J., Liu, Simin, Manson, JoAnn E., Meigs, James B., Waters, Kevin, Mukamal, Kenneth J., Pendergrass, Sarah A., Shrader, Peter, Wilkens, Lynne R., Hindorff, Lucia A., Ambite, Jose Luis, North, Kari E., Peters, Ulrike, Crawford, Dana C., Le Marchand, Loic, and Pankow, James S.

Published
2012
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24. Germline Sequencing DNA Repair Genes in 5545 Men With Aggressive and Nonaggressive Prostate Cancer

Author

Darst, Burcu F, primary, Dadaev, Tokhir, additional, Saunders, Ed, additional, Sheng, Xin, additional, Wan, Peggy, additional, Pooler, Loreall, additional, Xia, Lucy Y, additional, Chanock, Stephen, additional, Berndt, Sonja I, additional, Gapstur, Susan M, additional, Stevens, Victoria, additional, Albanes, Demetrius, additional, Weinstein, Stephanie J, additional, Gnanapragasam, Vincent, additional, Giles, Graham G, additional, Nguyen-Dumont, Tu, additional, Milne, Roger L, additional, Pomerantz, Mark, additional, Schmidt, Julie A, additional, Mucci, Lorelei, additional, Catalona, William J, additional, Hetrick, Kurt N, additional, Doheny, Kimberly F, additional, MacInnis, Robert J, additional, Southey, Melissa C, additional, Eeles, Rosalind A, additional, Wiklund, Fredrik, additional, Kote-Jarai, Zsofia, additional, Conti, David V, additional, and Haiman, Christopher A, additional

Published
2020
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25. The Four-Kallikrein Panel Is Effective in Identifying Aggressive Prostate Cancer in a Multiethnic Population

Author

Darst, Burcu F., primary, Chou, Alisha, additional, Wan, Peggy, additional, Pooler, Loreall, additional, Sheng, Xin, additional, Vertosick, Emily A., additional, Conti, David V., additional, Wilkens, Lynne R., additional, Le Marchand, Loïc, additional, Vickers, Andrew J., additional, Lilja, Hans G., additional, and Haiman, Christopher A., additional

Published
2020
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26. Population-specific reference panels are crucial for genetic analyses: an example of the CREBRF locus in Native Hawaiians

Author

Lin, Meng, primary, Caberto, Christian, additional, Wan, Peggy, additional, Li, Yuqing, additional, Lum-Jones, Annette, additional, Tiirikainen, Maarit, additional, Pooler, Loreall, additional, Nakamura, Brooke, additional, Sheng, Xin, additional, Porcel, Jacqueline, additional, Lim, Unhee, additional, Setiawan, Veronica Wendy, additional, Le Marchand, Loïc, additional, Wilkens, Lynne R, additional, Haiman, Christopher A, additional, Cheng, Iona, additional, and Chiang, Charleston W K, additional

Published
2020
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30. Germline Sequencing DNA Repair Genes in 5545 Men With Aggressive and Nonaggressive Prostate Cancer.

Author

Darst, Burcu F, Dadaev, Tokhir, Saunders, Ed, Sheng, Xin, Wan, Peggy, Pooler, Loreall, Xia, Lucy Y, Chanock, Stephen, Berndt, Sonja I, Gapstur, Susan M, Stevens, Victoria, Albanes, Demetrius, Weinstein, Stephanie J, Gnanapragasam, Vincent, Giles, Graham G, Nguyen-Dumont, Tu, Milne, Roger L, Pomerantz, Mark, Schmidt, Julie A, and Mucci, Lorelei

Subjects
DNA repair, GENES, HEREDITARY nonpolyposis colorectal cancer, GERM cells, PROSTATE cancer, ALLELES, BRCA genes, RESEARCH, GENETIC mutation, DNA, RESEARCH methodology, EVALUATION research, COMPARATIVE studies, DISEASE susceptibility, PROSTATE tumors
Abstract

Background: There is an urgent need to identify factors specifically associated with aggressive prostate cancer (PCa) risk. We investigated whether rare pathogenic, likely pathogenic, or deleterious (P/LP/D) germline variants in DNA repair genes are associated with aggressive PCa risk in a case-case study of aggressive vs nonaggressive disease.Methods: Participants were 5545 European-ancestry men, including 2775 nonaggressive and 2770 aggressive PCa cases, which included 467 metastatic cases (16.9%). Samples were assembled from 12 international studies and germline sequenced together. Rare (minor allele frequency < 0.01) P/LP/D variants were analyzed for 155 DNA repair genes. We compared single variant, gene-based, and DNA repair pathway-based burdens by disease aggressiveness. All statistical tests are 2-sided.Results: BRCA2 and PALB2 had the most statistically significant gene-based associations, with 2.5% of aggressive and 0.8% of nonaggressive cases carrying P/LP/D BRCA2 alleles (odds ratio [OR] = 3.19, 95% confidence interval [CI] = 1.94 to 5.25, P = 8.58 × 10-7) and 0.65% of aggressive and 0.11% of nonaggressive cases carrying P/LP/D PALB2 alleles (OR = 6.31, 95% CI = 1.83 to 21.68, P = 4.79 × 10-4). ATM had a nominal association, with 1.6% of aggressive and 0.8% of nonaggressive cases carrying P/LP/D ATM alleles (OR = 1.88, 95% CI = 1.10 to 3.22, P = .02). In aggregate, P/LP/D alleles within 24 literature-curated candidate PCa DNA repair genes were more common in aggressive than nonaggressive cases (carrier frequencies = 14.2% vs 10.6%, respectively; P = 5.56 × 10-5). However, this difference was non-statistically significant (P = .18) on excluding BRCA2, PALB2, and ATM. Among these 24 genes, P/LP/D carriers had a 1.06-year younger diagnosis age (95% CI = -1.65 to 0.48, P = 3.71 × 10-4).Conclusions: Risk conveyed by DNA repair genes is largely driven by rare P/LP/D alleles within BRCA2, PALB2, and ATM. These findings support the importance of these genes in both screening and disease management considerations. [ABSTRACT FROM AUTHOR]

Published
2021
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31. Estrogen-progestin replacement therapy and endometrial cancer

Author

Pike, Malcolm C., Peters, Ruth K., Cozen, Wendy, Probst-Hensch, Nicole M., Felix, Juan C., Wan, Peggy C., and Mack, Thomas M.

Subjects
Hormone therapy -- Evaluation, Endometrial cancer -- Risk factors, Progestational hormones -- Dosage and administration, Health
Abstract

Background: It has been known for more than 20 years that estrogen replacement therapy substantially increases a woman's risk of developing endometrial cancer. To reduce this increased risk, progestins have been added to estrogen replacement therapy for between 5 and 15 days (usually 7 or 10 days) per 'month' in a sequential fashion (sequential estrogen-progestin replacement therapy) or with each dose of estrogen replacement therapy (continuous combined replacement therapy). At the present time, however, little is known about the effects of varying the number of days that progestin is used in sequential estrogen-progestin replacement therapy. Purpose: We sought to determine the effects of sequential estrogen-progestin replacement therapy and continuous combined replacement therapy on a woman's risk of developing endometrial cancer. Methods: A population-based, case-control study of 833 case subjects and 791 control subjects was conducted. Women were postmenopausal, white, and aged 50-74 years when first diagnosed with invasive endometrial cancer or were aged 50-74 years at the matching date for control subjects. All subjects were interviewed in person with the aid of a month-by-month calendar. Relative risks were estimated by odds ratios (ORs); ORs were adjusted simultaneously for the different forms of hormone replacement therapy and for the known endometrial cancer risk factors. Results: The adjusted OR was 2.17 (95% confidence interval [CI] = 1.91-2.47) per 5 years of estrogen replacement therapy use (based on 422 users among the case subjects and 262 users among the control subjects). For women who received sequential estrogen-progestin replacement therapy with the progestin given for less than 10 days (effectively 7 days) per month, the adjusted OR was only slightly reduced to 1.87 (95% CI = 1.32-2.65) per 5 years of use (74 case subjects and 47 control subjects). However, when progestin was given for 10 or more days (effectively 10 days), there was essentially no increased risk (adjusted 0R = 1.07 per 5 years of use; 95% CI = 0.82-1.41) (79 case subjects and 88 control subjects). Continuous combined replacement therapy was also associated with essentially no increased risk (adjusted 0R = 1.07 per 5 years of use; 95% CI = 0.80-1.43) (94 case subjects and 81 control subjects). Conclusions: The progestin in sequential estrogen-progestin replacement therapy needs to be given for at least 10 days to block effectively any increased risk of endometrial cancer. Continuous combined estrogen-progestin therapy is similarly effective. Neither regimen reduces a woman's underlying risk of endometrial cancer. The sharp distinction between the effects of less than 10 days (effectively 7 days) and 10 or more days (effectively 10 days) of progestin use in sequential estrogen-progestin replacement therapy suggests that the extent of endometrial sloughing may play a critical role in determining endometrial cancer risk. [J Natl Cancer Inst 1997;89:1110-6]

Published
1997

32. Effect of Phytoestrogens from Soy Foods on Ovarian Function in Premenopausal Women

Author

Wu, Anna H., Stanczyk, Frank, Hendrich, Suzanne, Murphy, Patricia, Zhang, Chunying, Wan, Peggy, and Pike, Malcolm C.

Subjects
Soyfoods -- Health aspects, Breast cancer -- Risk factors, Estrogen -- Health aspects, Food/cooking/nutrition
Abstract

There is suggestive epidemiologic evidence that high soy intake may protect against breast cancer. The mechanisms by which intake of soy may influence risk of breast cancer are not known. A predominant hypothesis focuses on the potential effects of soy on hormone production and metabolism. The main objective of this soy intervention study was to investigate the relationship between ovarian function in healthy cycling premenopausal women and daily intake of Asian soy foods (tofu, soy milk and soybean peas). The women's hormone levels were compared during the soy intervention with their levels before and after intervention. Twenty women completed this 7-mo study, which consisted of 2 mo of baseline assessment, 3 mo of soyfood supplementation and 2 mo of follow-up assessment. During the entire study period, subjects provided morning urine specimens and blood specimens during specified days of their menstrual cycles. In addition, subjects completed a daily log to record information on menstrual cycle, alcohol intake, exercise pattern, and the amount and types of soy food eaten (during the intervention months only). Soy intervention was associated with a significant reduction in serum luteal estradiol level, but there were no significant changes in follicular phase estradiol, follicular or luteal phase progesterone, sex hormone--binding globulin or menstrual cycle length. Implications of these findings will be discussed.

Published
2000

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

Author

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

Abstract

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

Published
2011

35. A Genome-Wide Scan for Breast Cancer Risk Haplotypes among African American Women

Author

Song, Chi, primary, Chen, Gary K., additional, Millikan, Robert C., additional, Ambrosone, Christine B., additional, John, Esther M., additional, Bernstein, Leslie, additional, Zheng, Wei, additional, Hu, Jennifer J., additional, Ziegler, Regina G., additional, Nyante, Sarah, additional, Bandera, Elisa V., additional, Ingles, Sue A., additional, Press, Michael F., additional, Deming, Sandra L., additional, Rodriguez-Gil, Jorge L., additional, Chanock, Stephen J., additional, Wan, Peggy, additional, Sheng, Xin, additional, Pooler, Loreall C., additional, Van Den Berg, David J., additional, Le Marchand, Loic, additional, Kolonel, Laurence N., additional, Henderson, Brian E., additional, Haiman, Chris A., additional, and Stram, Daniel O., additional

Published
2013
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36. Evaluating Genetic Risk for Prostate Cancer among Japanese and Latinos

Author

Cheng, Iona, primary, Chen, Gary K., additional, Nakagawa, Hidewaki, additional, He, Jing, additional, Wan, Peggy, additional, Laurie, Cathy C., additional, Shen, Jess, additional, Sheng, Xin, additional, Pooler, Loreall C., additional, Crenshaw, Andrew T., additional, Mirel, Daniel B., additional, Takahashi, Atsushi, additional, Kubo, Michiaki, additional, Nakamura, Yusuke, additional, Al Olama, Ali Amin, additional, Benlloch, Sara, additional, Donovan, Jenny L., additional, Guy, Michelle, additional, Hamdy, Freddie C., additional, Kote-Jarai, Zsofia, additional, Neal, David E., additional, Wilkens, Lynne R., additional, Monroe, Kristine R., additional, Stram, Daniel O., additional, Muir, Kenneth, additional, Eeles, Rosalind A., additional, Easton, Douglas F., additional, Kolonel, Laurence N., additional, Henderson, Brian E., additional, Le Marchand, Loïc, additional, and Haiman, Christopher A., additional

Published
2012
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37. Reproducibility, Performance, and Clinical Utility of a Genetic Risk Prediction Model for Prostate Cancer in Japanese

Author

Akamatsu, Shusuke, primary, Takahashi, Atsushi, additional, Takata, Ryo, additional, Kubo, Michiaki, additional, Inoue, Takahiro, additional, Morizono, Takashi, additional, Tsunoda, Tatsuhiko, additional, Kamatani, Naoyuki, additional, Haiman, Christopher A., additional, Wan, Peggy, additional, Chen, Gary K., additional, Le Marchand, Loic, additional, Kolonel, Laurence N., additional, Henderson, Brian E., additional, Fujioka, Tomoaki, additional, Habuchi, Tomonori, additional, Nakamura, Yusuke, additional, Ogawa, Osamu, additional, and Nakagawa, Hidewaki, additional

Published
2012
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38. A genome-wide association study of breast cancer in women of African ancestry

Author

Chen, Fang, primary, Chen, Gary K., additional, Stram, Daniel O., additional, Millikan, Robert C., additional, Ambrosone, Christine B., additional, John, Esther M., additional, Bernstein, Leslie, additional, Zheng, Wei, additional, Palmer, Julie R., additional, Hu, Jennifer J., additional, Rebbeck, Tim R., additional, Ziegler, Regina G., additional, Nyante, Sarah, additional, Bandera, Elisa V., additional, Ingles, Sue A., additional, Press, Michael F., additional, Ruiz-Narvaez, Edward A., additional, Deming, Sandra L., additional, Rodriguez-Gil, Jorge L., additional, DeMichele, Angela, additional, Chanock, Stephen J., additional, Blot, William, additional, Signorello, Lisa, additional, Cai, Qiuyin, additional, Li, Guoliang, additional, Long, Jirong, additional, Huo, Dezheng, additional, Zheng, Yonglan, additional, Cox, Nancy J., additional, Olopade, Olufunmilayo I., additional, Ogundiran, Temidayo O., additional, Adebamowo, Clement, additional, Nathanson, Katherine L., additional, Domchek, Susan M., additional, Simon, Michael S., additional, Hennis, Anselm, additional, Nemesure, Barbara, additional, Wu, Suh-Yuh, additional, Leske, M. Cristina, additional, Ambs, Stefan, additional, Hutter, Carolyn M., additional, Young, Alicia, additional, Kooperberg, Charles, additional, Peters, Ulrike, additional, Rhie, Suhn K., additional, Wan, Peggy, additional, Sheng, Xin, additional, Pooler, Loreall C., additional, Van Den Berg, David J., additional, Le Marchand, Loic, additional, Kolonel, Laurence N., additional, Henderson, Brian E., additional, and Haiman, Christopher A., additional

Published
2012
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39. Characterizing Genetic Risk at Known Prostate Cancer Susceptibility Loci in African Americans

Author

Haiman, Christopher A., primary, Chen, Gary K., additional, Blot, William J., additional, Strom, Sara S., additional, Berndt, Sonja I., additional, Kittles, Rick A., additional, Rybicki, Benjamin A., additional, Isaacs, William B., additional, Ingles, Sue A., additional, Stanford, Janet L., additional, Diver, W. Ryan, additional, Witte, John S., additional, Chanock, Stephen J., additional, Kolb, Suzanne, additional, Signorello, Lisa B., additional, Yamamura, Yuko, additional, Neslund-Dudas, Christine, additional, Thun, Michael J., additional, Murphy, Adam, additional, Casey, Graham, additional, Sheng, Xin, additional, Wan, Peggy, additional, Pooler, Loreall C., additional, Monroe, Kristine R., additional, Waters, Kevin M., additional, Le Marchand, Loic, additional, Kolonel, Laurence N., additional, Stram, Daniel O., additional, and Henderson, Brian E., additional

Published
2011
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43. Response

Author

Pike, Malcolm C., primary, Peters, Ruth K., additional, Cozen, Wendy, additional, Probst-Hensch, Nicole M., additional, Felix, Juan C., additional, Wan, Peggy C., additional, and Mack, Thomas M., additional

Published
1998
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44. Adolescent and adult soy intake and risk of breast cancer in Asian-Americans.

Author

Wu, Anna H, Wan, Peggy, Hankin, Jean, Tseng, Chiu-Chen, Yu, Mimi C, and Pike, Malcolm C

Abstract

The association between soyfood intake and breast cancer risk is controversial. Most of the epidemiologic studies published on this topic in the 1990s were not designed to specifically address this question. We conducted a population-based, case-control study of breast cancer among Chinese, Japanese and Filipino women in Los Angeles County to further investigate the role of soy. Our primary objective was to quantify breast cancer risks associated with intake of soy during adolescence and adult life among Asian-American women. During 1995-1998, we successfully interviewed 501 breast cancer patients and 594 control subjects. Intake of soy among Asian-Americans is still relatively high; the median intake was 12 mg isoflavones/day, approximately one-third of that reported in a recent study in Shanghai, China. The risk of breast cancer was significantly inversely associated with soy intake during adolescence and adult life. After adjusting for age, specific Asian ethnicity, education, migration history and menstrual and reproductive factors, women who reported soy intake at least once per week during adolescence showed a statistically significantly reduced risk of breast cancer. There was also a significant trend of decreasing risk with increasing soy intake during adult life. When we considered soy intake during both adolescence and adult life, subjects who were high-soy consumers during both time periods showed the lowest risk (OR=0.53, 95% CI=0.36-0.78) compared with those who were low consumers during both time periods. Risk of breast cancer was intermediate among subjects who were high-soy consumers during adolescence and low-soy consumers during adult life (OR=0.77, 95% CI=0.51-1.10). Based on a relatively small number of subjects, the risk did not appear to differ between those who were low consumers during adolescence and high consumers during adult life. Results remained similar after adjustment for other potential confounders including other dietary and non-dietary risk factors for breast cancer. These results show that high soy intake in childhood in Asian-Americans is associated with reduced breast cancer risk. Risk may be further reduced by intake as an adult.

Published
2002
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45. The Four-Kallikrein Panel Is Effective in Identifying Aggressive Prostate Cancer in a Multiethnic Population.

Author

Darst, Burcu F., Chou, Alisha, Wan, Peggy, Pooler, Loreall, Xin Sheng, Vertosick, Emily A., Conti, David V., Wilkens, Lynne R., Le Marchand, Loïc, Vickers, Andrew J., Lilja, Hans G., and Haiman, Christopher A.

Abstract

Background: The four-kallikrein (4K) panel has been demonstrated to improve prediction of aggressive prostate cancer compared with prostate-specific antigen (PSA) among men with moderately elevated PSA levels. However, the development and testing of the 4K panel has been conducted primarily in White men, with limited data in African Americans and no studies in other racial and ethnic groups. Methods: We evaluated the 4K panel in a nested case-control study among African American, Latino, Japanese, Native Hawaiian, and White men in the Multiethnic Cohort. Prediagnostic blood levels of free, intact, and total PSA and human kallikrein-related peptidase 2 were measured among 1,667 incident prostate cancer cases and 691 controls with PSA ≥2 ng/mL. We evaluated the discriminative ability of the 4K panel within and across all racial/ethnic groups. Results: The 4K panel enhanced discrimination of overall prostate cancer compared with free plus total PSA and total PSA alone (AUC 0.748 vs. 0.711 and 0.669, respectively). Discrimination was further enhanced for Gleason 8+ prostate cancer, aggressive prostate cancer, and death due to prostate cancer, and to a lesser degree for nonaggressive prostate cancer. Improvement of the 4K panel over PSA was observed in each population. Adding a prostate cancer polygenic risk score slightly improved upon the discriminative ability of the 4K panel. Conclusions: The superior discriminative ability of the 4K panel over PSA for overall and aggressive prostate cancer across multiethnic populations indicates the broad clinical applicability of the 4K panel. Impact: Our multiethnic investigation suggests potential for the 4K panel to improve current prostate cancer screening practices. [ABSTRACT FROM AUTHOR]

Published
2020
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46. Germline Sequencing DNA Repair Genes in 5545 Men With Aggressive and Nonaggressive Prostate Cancer.

Author

Darst BF, Dadaev T, Saunders E, Sheng X, Wan P, Pooler L, Xia LY, Chanock S, Berndt SI, Gapstur SM, Stevens V, Albanes D, Weinstein SJ, Gnanapragasam V, Giles GG, Nguyen-Dumont T, Milne RL, Pomerantz M, Schmidt JA, Mucci L, Catalona WJ, Hetrick KN, Doheny KF, MacInnis RJ, Southey MC, Eeles RA, Wiklund F, Kote-Jarai Z, Conti DV, and Haiman CA

Subjects
DNA Repair genetics, Genes, BRCA2, Genetic Predisposition to Disease, Germ Cells pathology, Humans, Male, Germ-Line Mutation, Prostatic Neoplasms pathology
Abstract

Background: There is an urgent need to identify factors specifically associated with aggressive prostate cancer (PCa) risk. We investigated whether rare pathogenic, likely pathogenic, or deleterious (P/LP/D) germline variants in DNA repair genes are associated with aggressive PCa risk in a case-case study of aggressive vs nonaggressive disease., Methods: Participants were 5545 European-ancestry men, including 2775 nonaggressive and 2770 aggressive PCa cases, which included 467 metastatic cases (16.9%). Samples were assembled from 12 international studies and germline sequenced together. Rare (minor allele frequency < 0.01) P/LP/D variants were analyzed for 155 DNA repair genes. We compared single variant, gene-based, and DNA repair pathway-based burdens by disease aggressiveness. All statistical tests are 2-sided., Results: BRCA2 and PALB2 had the most statistically significant gene-based associations, with 2.5% of aggressive and 0.8% of nonaggressive cases carrying P/LP/D BRCA2 alleles (odds ratio [OR] = 3.19, 95% confidence interval [CI] = 1.94 to 5.25, P = 8.58 × 10-7) and 0.65% of aggressive and 0.11% of nonaggressive cases carrying P/LP/D PALB2 alleles (OR = 6.31, 95% CI = 1.83 to 21.68, P = 4.79 × 10-4). ATM had a nominal association, with 1.6% of aggressive and 0.8% of nonaggressive cases carrying P/LP/D ATM alleles (OR = 1.88, 95% CI = 1.10 to 3.22, P = .02). In aggregate, P/LP/D alleles within 24 literature-curated candidate PCa DNA repair genes were more common in aggressive than nonaggressive cases (carrier frequencies = 14.2% vs 10.6%, respectively; P = 5.56 × 10-5). However, this difference was non-statistically significant (P = .18) on excluding BRCA2, PALB2, and ATM. Among these 24 genes, P/LP/D carriers had a 1.06-year younger diagnosis age (95% CI = -1.65 to 0.48, P = 3.71 × 10-4)., Conclusions: Risk conveyed by DNA repair genes is largely driven by rare P/LP/D alleles within BRCA2, PALB2, and ATM. These findings support the importance of these genes in both screening and disease management considerations., (© The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2021
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47. Breast cancer in a multiethnic cohort in Hawaii and Los Angeles: risk factor-adjusted incidence in Japanese equals and in Hawaiians exceeds that in whites.

Author

Pike MC, Kolonel LN, Henderson BE, Wilkens LR, Hankin JH, Feigelson HS, Wan PC, Stram DO, and Nomura AM

Subjects
Aged, Cohort Studies, Female, Hawaii epidemiology, Humans, Incidence, Los Angeles epidemiology, Middle Aged, Postmenopause, Risk Factors, Asian statistics & numerical data, Breast Neoplasms epidemiology, Breast Neoplasms ethnology, Hispanic or Latino statistics & numerical data, White People statistics & numerical data
Abstract

Few data exist on the extent to which the differences in breast cancer risk between "racial-ethnic" groups in the United States (US) are "explained" by differences in their distribution of risk factors. We have determined this for African-American (AA), native Hawaiian (NH), Japanese-American (JA), Latina-US-born (L-US), Latina-non-US-born (L-NUS), and white (W) women using prospective incidence data on 88,712 postmenopausal women recruited in 1993-1996. We identified 1,757 incident breast cancer cases through 1999 among these women (1,116 cases after excluding women with a simple hysterectomy or missing risk factor data). Data were available on seven "known" risk factors: ages at menarche and first birth; parity; age at and type of menopause; weight; hormone replacement therapy use; and alcohol consumption. The relative risks (RRs) of breast cancer (with the RR in Ws set to 1.0) for the groups were as follows: W = 1.0; AA = 0.78; NH = 1.33; JA = 0.99; L-US = 0.77; and L-NUS = 0.60. After adjustment for the risk factors, the RRs were as follows: W = 1.0; AA = 0.98; NH = 1.65; JA = 1.11; L-US = 0.95; and L-NUSB = 0.84. The slightly greater risk of the JAs compared with the Ws is in sharp contrast to the very low breast cancer rates that were observed in "traditional" Japanese women and in early Japanese migrants. The adjusted RR of NHs is 65% greater than that of Ws, and that of migrant Latinas is 16% lower than that of Ws. Elucidating the causes of the high rates in NHs is now a major focus of our efforts.

Published
2002

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