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1. Assessment of polygenic architecture and risk prediction based on common variants across fourteen cancers

Author

Zhang, Yan Dora, Hurson, Amber N, Zhang, Haoyu, Choudhury, Parichoy Pal, Easton, Douglas F, Milne, Roger L, Simard, Jacques, Hall, Per, Michailidou, Kyriaki, Dennis, Joe, Schmidt, Marjanka K, Chang-Claude, Jenny, Gharahkhani, Puya, Whiteman, David, Campbell, Peter T, Hoffmeister, Michael, Jenkins, Mark, Peters, Ulrike, Hsu, Li, Gruber, Stephen B, Casey, Graham, Schmit, Stephanie L, O'Mara, Tracy A, Spurdle, Amanda B, Thompson, Deborah J, Tomlinson, Ian, De Vivo, Immaculata, Landi, Maria Teresa, Law, Matthew H, Iles, Mark M, Demenais, Florence, Kumar, Rajiv, MacGregor, Stuart, Bishop, D Timothy, Ward, Sarah V, Bondy, Melissa L, Houlston, Richard, Wiencke, John K, Melin, Beatrice, Barnholtz-Sloan, Jill, Kinnersley, Ben, Wrensch, Margaret R, Amos, Christopher I, Hung, Rayjean J, Brennan, Paul, McKay, James, Caporaso, Neil E, Berndt, Sonja I, Birmann, Brenda M, Camp, Nicola J, Kraft, Peter, Rothman, Nathaniel, Slager, Susan L, Berchuck, Andrew, Pharoah, Paul DP, Sellers, Thomas A, Gayther, Simon A, Pearce, Celeste L, Goode, Ellen L, Schildkraut, Joellen M, Moysich, Kirsten B, Amundadottir, Laufey T, Jacobs, Eric J, Klein, Alison P, Petersen, Gloria M, Risch, Harvey A, Stolzenberg-Solomon, Rachel Z, Wolpin, Brian M, Li, Donghui, Eeles, Rosalind A, Haiman, Christopher A, Kote-Jarai, Zsofia, Schumacher, Fredrick R, Al Olama, Ali Amin, Purdue, Mark P, Scelo, Ghislaine, Dalgaard, Marlene D, Greene, Mark H, Grotmol, Tom, Kanetsky, Peter A, McGlynn, Katherine A, Nathanson, Katherine L, Turnbull, Clare, Wiklund, Fredrik, Breast Cancer Association Consortium (BCAC), Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON), Colon Cancer Family Registry (CCFR), Transdisciplinary Studies of Genetic Variation in Colorectal Cancer (CORECT), Endometrial Cancer Association Consortium (ECAC), Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), Melanoma Genetics Consortium (GenoMEL), Glioma International Case-Control Study (GICC), International Lung Cancer Consortium (ILCCO), Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium, International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies (InterLymph), Ovarian Cancer Association Consortium (OCAC), Oral Cancer GWAS, Pancreatic Cancer Case-Control Consortium (PanC4), Pancreatic Cancer Cohort Consortium (PanScan), and Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL)

Subjects
Male, Urologic Diseases, Multifactorial Inheritance, Ovarian Cancer Association Consortium, Risk Assessment, Transdisciplinary Studies of Genetic Variation in Colorectal Cancer, Genetic, Risk Factors, Models, Neoplasms, Genetics, Animals, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Endometrial Cancer Association Consortium, Aetiology, Polymorphism, International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies, Cancer, Renal Cancer GWAS, Incidence, Prevention, Prostate Cancer, International Lung Cancer Consortium, Human Genome, Melanoma Genetics Consortium, Single Nucleotide, Barrett’s and Esophageal Adenocarcinoma Consortium, Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome, Genetics and Epidemiology of Colorectal Cancer Consortium, Pancreatic Cancer Case-Control Consortium, Testicular Cancer Consortium, Breast Cancer Association Consortium, Oral Cancer GWAS, Female, Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium, Colon Cancer Family Registry, Glioma International Case-Control Study, Pancreatic Cancer Cohort Consortium, Genome-Wide Association Study
Abstract

Genome-wide association studies (GWAS) have led to the identification of hundreds of susceptibility loci across cancers, but the impact of further studies remains uncertain. Here we analyse summary-level data from GWAS of European ancestry across fourteen cancer sites to estimate the number of common susceptibility variants (polygenicity) and underlying effect-size distribution. All cancers show a high degree of polygenicity, involving at a minimum of thousands of loci. We project that sample sizes required to explain 80% of GWAS heritability vary from 60,000 cases for testicular to over 1,000,000 cases for lung cancer. The maximum relative risk achievable for subjects at the 99th risk percentile of underlying polygenic risk scores (PRS), compared to average risk, ranges from 12 for testicular to 2.5 for ovarian cancer. We show that PRS have potential for risk stratification for cancers of breast, colon and prostate, but less so for others because of modest heritability and lower incidence.

Published
2020

2. Exogenous hormone use, reproductive factors and risk of intrahepatic cholangiocarcinoma among women: results from cohort studies in the Liver Cancer Pooling Project and the UK Biobank

Author

Petrick, Jessica L, McMenamin, Úna C, Zhang, Xuehong, Zeleniuch-Jacquotte, Anne, Wactawski-Wende, Jean, Simon, Tracey G, Sinha, Rashmi, Sesso, Howard D, Schairer, Catherine, Rosenberg, Lynn, Rohan, Thomas E, Robien, Kim, Purdue, Mark P, Poynter, Jenny N, Palmer, Julie R, Lu, Yunxia, Linet, Martha S, Liao, Linda M, Lee, I-Min, Koshiol, Jill, Kitahara, Cari M, Kirsh, Victoria A, Hofmann, Jonathan N, Graubard, Barry I, Giovannucci, Edward, Gaziano, J Michael, Gapstur, Susan M, Freedman, Neal D, Florio, Andrea A, Chong, Dawn Q, Chen, Yu, Chan, Andrew T, Buring, Julie E, Freeman, Laura E Beane, Bea, Jennifer W, Cardwell, Christopher R, Campbell, Peter T, and McGlynn, Katherine A

Subjects
Oral, Liver Cancer, Oncology and Carcinogenesis, Reproductive health and childbirth, Hysterectomy, Cholangiocarcinoma, Cohort Studies, Rare Diseases, Risk Factors, Clinical Research, Humans, Estrogen Receptor beta, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Aetiology, Digestive Diseases - (Gallbladder), Proportional Hazards Models, Aged, Biological Specimen Banks, Cancer, Intrahepatic, Neoplastic, Hormonal, Prevention, Liver Disease, Contraception/Reproduction, Liver Neoplasms, Estrogen Receptor alpha, Contraceptives, Middle Aged, Hormones, United Kingdom, Good Health and Well Being, Gene Expression Regulation, Public Health and Health Services, Female, Bile Ducts, Menopause, Digestive Diseases
Abstract

BackgroundIntrahepatic cholangiocarcinoma (ICC) arises from cholangiocytes in the intrahepatic bile duct and is the second most common type of liver cancer. Cholangiocytes express both oestrogen receptor-α and -β, and oestrogens positively modulate cholangiocyte proliferation. Studies in women and men have reported higher circulating oestradiol is associated with increased ICC risk, further supporting a hormonal aetiology. However, no observational studies have examined the associations between exogenous hormone use and reproductive factors, as proxies of endogenous hormone levels, and risk of ICC.MethodsWe harmonised data from 1,107,498 women who enroled in 12 North American-based cohort studies (in the Liver Cancer Pooling Project, LCPP) and the UK Biobank between 1980-1998 and 2006-2010, respectively. Cox proportional hazards regression models were used to generate hazard ratios (HR) and 95% confidence internals (CI). Then, meta-analytic techniques were used to combine the estimates from theLCPP (n = 180 cases) and the UK Biobank (n = 57 cases).ResultsHysterectomy was associated with a doubling of ICC risk (HR = 1.98,95%CI:1.27-3.09), compared to women aged 50-54 at natural menopause. Long-term oral contraceptive use (9+ years) was associated with a 62% increased ICC risk (HR = 1.62,95%CI:1.03-2.55). There was no association between ICC risk and other exogenous hormone use or reproductive factors.ConclusionsThis study suggests that hysterectomy and long-term oral contraceptive use may be associated with an increased ICC risk.

Published
2020

3. Additional file 2 of Leukemia mortality in children from Latin America: trends and predictions to 2030

Author

Torres-Roman, J. Smith, Valcarcel, Bryan, Guerra-Canchari, Pedro, Santos, Camila Alves Dos, Barbosa, Isabelle Ribeiro, Vecchia, Carlo La, McGlynn, Katherine A., and Dyego Leandro Bezerra De Souza

Subjects
sense organs
Abstract

Additional file 2: Supplementary 2. Estimated annual percent change (EAPC, %) and 95% confidence interval (CI) for leukemia mortality rates in 0–14 years.

Published
2020
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4. Additional file 1 of Leukemia mortality in children from Latin America: trends and predictions to 2030

Author

Torres-Roman, J. Smith, Valcarcel, Bryan, Guerra-Canchari, Pedro, Santos, Camila Alves Dos, Barbosa, Isabelle Ribeiro, Vecchia, Carlo La, McGlynn, Katherine A., and Dyego Leandro Bezerra De Souza

Subjects
sense organs
Abstract

Additional file 1: Supplementary 1. Age-standardized mortality rates from leukemia in children from Latin America and the Caribbean in the periods 2000–2005, and 2012–2017, and corresponding percent changes.

Published
2020
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5. Additional file 1: of Physical activity and risk of testicular cancer: a systematic review

Author

Huang, Stephanie, Signal, Virginia, Sarfati, Diana, Shaw, Caroline, Stanley, James, McGlynn, Katherine, and Gurney, Jason

Abstract

Table S1. Papers included in meta-analysis of association between physical activity and testicular cancer risk, with study meta-data. Table S2. Extracted data relating to high vs. low physical activity. Table S3. Extracted data relating to high vs. low recreational physical activity at adolescence/early adulthood. Table S4. PICOS (Patient/Participant, Intervention, Comparator, Outcome, Study design) criteria for inclusion of studies. Table S5. List of excluded papers with reason for exclusion. Table S6. Assessment of study quality against Newcastle-Ottawa criteria for case-control studies. Table S7. Assessment of study quality against Newcastle-Ottawa criteria for cohort studies. (DOCX 134Â kb)

Published
2018
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6. Meta-analysis of five genome-wide association studies identifies multiple new loci associated with testicular germ cell tumor

Author

Wang, Zhaoming, Mcglynn, Katherine A, Rajpert De Meyts, Ewa, Bishop, D. Timothy, Chung, Charles C, Dalgaard, Marlene D, Greene, Mark H, Gupta, Ramneek, Grotmol, Tom, Haugen, Trine B, Karlsson, Robert, Litchfield, Kevin, Mitra, Nandita, Nielsen, Kasper, Pyle, Louise C, Schwartz, Stephen M, Thorsson, Vésteinn, Vardhanabhuti, Saran, Wiklund, Fredrik, Turnbull, Clare, Chanock, Stephen J, Kanetsky, Peter A, Nathanson, Katherine L, Testicular Cancer Consortium: McGlynn KA, Rajpert De Meyts, E, Bishop, Dt, Greene, Mh, Gupta, R, Grotmol, T, Haugen, Tb, Schwartz, Sm, Wiklund, F, Turnbull, C, Chanock, Sj, Kanetsky, Pa, Nathanson, Kl, Ferlin, Alberto, Gietema, Ja, Cortessis, V, Hauser, R, Hildebrandt, M, Kiemeney, La, Kubisch, C, Lessel, D, Rafnar, T, Richiardi, L, Skotheim, R, Zheng, T., Guided Treatment in Optimal Selected Cancer Patients (GUTS), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)

Subjects
0301 basic medicine, Male, Genome-wide association study, Disease, VARIANTS, Genome-wide association studies, DISEASE, 0302 clinical medicine, Genotype, FAMILIAL RISK, Genetics, HERITABILITY, Chromosome Mapping, Neoplasms, Germ Cell and Embryonal, 3. Good health, 030220 oncology & carcinogenesis, CARCINOMA IN-SITU, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], EXPRESSION, Adult, Genetic Markers, Risk, SUSCEPTIBILITY LOCI, Testicular Germ Cell Tumor, RELATIVES, Meta-analysises, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Young Adult, Testicular Neoplasms, medicine, Humans, Computer Simulation, Genetic Predisposition to Disease, Testicular cancer, Genetic association, Family Health, Chromosomes, Human, X, Haplotype, Computational Biology, medicine.disease, COMPONENT, 030104 developmental biology, Haplotypes, Genetic marker, CANCER INCIDENCE, Testicular germ cell tumors, Genome-Wide Association Study
Abstract

Item does not contain fulltext The international Testicular Cancer Consortium (TECAC) combined five published genome-wide association studies of testicular germ cell tumor (TGCT; 3,558 cases and 13,970 controls) to identify new susceptibility loci. We conducted a fixed-effects meta-analysis, including, to our knowledge, the first analysis of the X chromosome. Eight new loci mapping to 2q14.2, 3q26.2, 4q35.2, 7q36.3, 10q26.13, 15q21.3, 15q22.31, and Xq28 achieved genome-wide significance (P < 5 x 10-8). Most loci harbor biologically plausible candidate genes. We refined previously reported associations at 9p24.3 and 19p12 by identifying one and three additional independent SNPs, respectively. In aggregate, the 39 independent markers identified to date explain 37% of father-to-son familial risk, 8% of which can be attributed to the 12 new signals reported here. Our findings substantially increase the number of known TGCT susceptibility alleles, move the field closer to a comprehensive understanding of the underlying genetic architecture of TGCT, and provide further clues to the etiology of TGCT.

Published
2016

7. Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types

Author

Sampson, Joshua N, Wheeler, William A, Yeager, Meredith, Panagiotou, Orestis, Wang, Zhaoming, Berndt, Sonja I, Lan, Qing, Abnet, Christian C, Amundadottir, Laufey T, Figueroa, Jonine D, Landi, Maria Teresa, Mirabello, Lisa, Savage, Sharon A, Taylor, Philip R, De Vivo, Immaculata, McGlynn, Katherine A, Purdue, Mark P, Rajaraman, Preetha, Adami, Hans-Olov, Ahlbom, Anders, Albanes, Demetrius, Amary, Maria Fernanda, An, She-Juan, Andersson, Ulrika, Andriole, Gerald, Andrulis, Irene L, Angelucci, Emanuele, Ansell, Stephen M, Arici, Cecilia, Armstrong, Bruce K, Arslan, Alan A, Austin, Melissa A, Baris, Dalsu, Barkauskas, Donald A, Bassig, Bryan A, Becker, Nikolaus, Benavente, Yolanda, Benhamou, Simone, Berg, Christine, Van Den Berg, David, Bernstein, Leslie, Bertrand, Kimberly A, Birmann, Brenda M, Black, Amanda, Boeing, Heiner, Boffetta, Paolo, Boutron-Ruault, Marie-Christine, Bracci, Paige M, Brinton, Louise, Brooks-Wilson, Angela R, Bueno-de-Mesquita, H Bas, Burdett, Laurie, Buring, Julie, Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chan, John KC, Chang, Ellen T, Chang, Gee-Chen, Chang, I-Shou, Chang, Jiang, Chang-Claude, Jenny, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chu, Chen, Chung-Hsing, Chen, Constance, Chen, Hongyan, Chen, Kexin, Chen, Kuan-Yu, Chen, Kun-Chieh, Chen, Ying, Chen, Ying-Hsiang, Chen, Yi-Song, Chen, Yuh-Min, Chien, Li-Hsin, Chirlaque, María-Dolores, Choi, Jin Eun, Choi, Yi Young, Chow, Wong-Ho, Chung, Charles C, Clavel, Jacqueline, Clavel-Chapelon, Françoise, Cocco, Pierluigi, Colt, Joanne S, Comperat, Eva, Conde, Lucia, Connors, Joseph M, Conti, David, Cortessis, Victoria K, Cotterchio, Michelle, Cozen, Wendy, Crouch, Simon, Crous-Bou, Marta, Cussenot, Olivier, and Davis, Faith G

Subjects
Adult, Asian Continental Ancestry Group, Male, Lung Neoplasms, Lymphoma, European Continental Ancestry Group, Oncology and Carcinogenesis, Bone Neoplasms, Testicular Neoplasms, Neoplasms, Large B-Cell, Humans, Genetic Predisposition to Disease, Oncology & Carcinogenesis, Polymorphism, Chronic, Aged, Osteosarcoma, Leukemia, Smoking, B-Cell, Single Nucleotide, Middle Aged, Diffuse, Kidney Neoplasms, Lymphocytic, Urinary Bladder Neoplasms, Tissue Array Analysis, Female, Genome-Wide Association Study
Abstract

BackgroundStudies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.MethodsBetween 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.ResultsGWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.ConclusionOur results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.

Published
2015

8. Circulating total testosterone and PSA concentrations in a nationally representative sample of men without a diagnosis of prostate cancer

Author

Peskoe, Sarah B, Joshu, Corinne E, Rohrmann, Sabine, McGlynn, Katherine A, Nyante, Sarah J, Bradwin, Gary, Dobs, Adrian S, Kanarek, Norma, Nelson, William G, Platz, Elizabeth A, University of Zurich, and Platz, Elizabeth A

Subjects
2748 Urology, 610 Medicine & health, 2730 Oncology, 10060 Epidemiology, Biostatistics and Prevention Institute (EBPI)
Published
2015
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10. Detectable clonal mosaicism and its relationship to aging and cancer

Author

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

Subjects
Aging, Envelliment, Càncer, Cancer
Abstract

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

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