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Clonal hematopoiesis and risk of prostate cancer in large samples of European ancestry men.
Wang, Anqi; Xu, Yili; Yu, Yao; Nead, Kevin T; Kim, TaeBeom; Xu, Keren; 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 M; Schmidt, Julie A; Stopsack, Konrad H; Mucci, Lorelei A; Catalona, William J; Hetrick, Kurt N; Doheny, Kimberly F; MacInnis, Robert J; Southey, Melissa C; Eeles, Rosalind A; Wiklund, Fredrik; Kote-Jarai, Zsofia; de Smith, Adam J; Conti, David V; Huff, Chad; Haiman, Christopher A; Darst, Burcu F.
Afiliación
  • Wang A; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Xu Y; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Yu Y; Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77230, USA.
  • Nead KT; Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77230, USA.
  • Kim T; Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77230, USA.
  • Xu K; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Dadaev T; The Institute of Cancer Research, London, SM2 5NG, UK.
  • Saunders E; The Institute of Cancer Research, London, SM2 5NG, UK.
  • Sheng X; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Wan P; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Pooler L; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Xia LY; Department of Population and Public Health Sciences, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
  • Chanock S; National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Berndt SI; National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Gapstur SM; American Cancer Society, Atlanta, GA 30303, USA.
  • Stevens V; American Cancer Society, Atlanta, GA 30303, USA.
  • Albanes D; National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Weinstein SJ; National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Gnanapragasam V; Division of Urology, Department of Surgery, University of Cambridge, Cambridge, CB2 0QQ, UK.
  • Giles GG; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria 3004, Australia.
  • Nguyen-Dumont T; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Victoria 3168, Australia.
  • Milne RL; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Victoria 3010, Australia.
  • Pomerantz MM; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Victoria 3168, Australia.
  • Schmidt JA; Department of Clinical Pathology, The University of Melbourne, Victoria 3010, Australia.
  • Stopsack KH; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria 3004, Australia.
  • Mucci LA; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Victoria 3168, Australia.
  • Catalona WJ; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Victoria 3010, Australia.
  • Hetrick KN; Dana-Farber Cancer Institute, Boston, MA 02215, USA.
  • Doheny KF; Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, OX3 7LF, UK.
  • MacInnis RJ; Department of Clinical Epidemiology, Department of Clinical Medicine, Aarhus University Hospital and Aarhus University, Aarhus N, DK-8200, Denmark.
  • Southey MC; Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
  • Eeles RA; Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
  • Wiklund F; Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
  • Kote-Jarai Z; Department of Genetic Medicine, Center for Inherited Disease Research, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
  • de Smith AJ; Department of Genetic Medicine, Center for Inherited Disease Research, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
  • Conti DV; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria 3004, Australia.
  • Huff C; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, University of Melbourne, Victoria 3010, Australia.
  • Haiman CA; Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria 3004, Australia.
  • Darst BF; Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Victoria 3168, Australia.
Hum Mol Genet ; 32(3): 489-495, 2023 01 13.
Article en En | MEDLINE | ID: mdl-36018819
ABSTRACT
Little is known regarding the potential relationship between clonal hematopoiesis (CH) of indeterminate potential (CHIP), which is the expansion of hematopoietic stem cells with somatic mutations, and risk of prostate cancer, the fifth leading cause of cancer death of men worldwide. We evaluated the association of age-related CHIP with overall and aggressive prostate cancer risk in two large whole-exome sequencing studies of 75 047 European ancestry men, including 7663 prostate cancer cases, 2770 of which had aggressive disease, and 3266 men carrying CHIP variants. We found that CHIP, defined by over 50 CHIP genes individually and in aggregate, was not significantly associated with overall (aggregate HR = 0.93, 95% CI = 0.76-1.13, P = 0.46) or aggressive (aggregate OR = 1.14, 95% CI = 0.92-1.41, P = 0.22) prostate cancer risk. CHIP was weakly associated with genetic risk of overall prostate cancer, measured using a polygenic risk score (OR = 1.05 per unit increase, 95% CI = 1.01-1.10, P = 0.01). CHIP was not significantly associated with carrying pathogenic/likely pathogenic/deleterious variants in DNA repair genes, which have previously been found to be associated with aggressive prostate cancer. While findings from this study suggest that CHIP is likely not a risk factor for prostate cancer, it will be important to investigate other types of CH in association with prostate cancer risk.
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Texto completo: 1 Base de datos: MEDLINE Asunto principal: Neoplasias de la Próstata / Hematopoyesis Clonal Tipo de estudio: Etiology_studies / Risk_factors_studies Idioma: En Revista: Hum Mol Genet Asunto de la revista: BIOLOGIA MOLECULAR / GENETICA MEDICA Año: 2023 Tipo del documento: Article
Texto completo
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Texto completo: 1 Base de datos: MEDLINE Asunto principal: Neoplasias de la Próstata / Hematopoyesis Clonal Tipo de estudio: Etiology_studies / Risk_factors_studies Idioma: En Revista: Hum Mol Genet Asunto de la revista: BIOLOGIA MOLECULAR / GENETICA MEDICA Año: 2023 Tipo del documento: Article