Sarah C Markt1, Irene M Shui1,2, Robert H Unger1, Yuksel Urun3, Christine D Berg4, Amanda Black5, Paul Brennan6, H Bas Bueno-de-Mesquita7,8,9,10, Susan M Gapstur11, Edward Giovannucci1,12, Christopher Haiman13, Brian Henderson13, Robert N Hoover6, David J Hunter1,2,14, Timothy J Key15, Kay-Tee Khaw16, Federico Canzian17, Nerea Larranga18,19, Loic Le Marchand20, Jing Ma1,21, Alessio Naccarati22, Afshan Siddiq23, Meir J Stampfer1,21, Par Stattin24, Victoria L Stevens12, Daniel O Stram13, Anne Tjønneland25, Ruth C Travis15, Dimitrios Trichopoulos1,26,27, Regina G Ziegler6, Sara Lindstrom1,14, Peter Kraft1,14, Lorelei A Mucci1,21, Toni K Choueiri28, Kathryn M Wilson1. 1. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts. 2. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. 3. Department of Medical Oncology, Ankara University Faculty of Medicine, Ankara, Turkey. 4. Department of Radiation Oncology, Johns Hopkins Medicine, Baltimore, Maryland. 5. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland. 6. International Agency for Research on Cancer, Lyon, France. 7. National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. 8. Departments of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands. 9. Departments of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, UK. 10. Departments of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. 11. Epidemiology Research Program, American Cancer Society, Atlanta, Georgia. 12. Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, Massachusetts. 13. Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California. 14. Program in Genetic Epidemiology and Statistical Genetics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 15. Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. 16. School of Clinical Medicine, Cambridge Institute of Public Health, University of Cambridge, Cambridge, UK. 17. Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. 18. Public Health Division of Gipuzkoa, BIODonostia Research Institute, Basque Health Department, Spain. 19. CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain. 20. Epidemiology Program, University of Hawaii Cancer Center, Honolulu, Hawaii. 21. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. 22. HuGeF Foundation Molecular and Genetic Epidemiology Unit, Torino, Italy. 23. Department of Genomics of Common Disease, School of Public Health, Imperial College London, London, UK. 24. Department of Surgery and Perioperative sciences, Urology and Andrology, Ume, å, University, Sweden. 25. Danish Cancer Society Research Center, Copenhagen, Denmark. 26. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. 27. Hellenic Health Foundation, Athens, Greece. 28. Department of Genitourinary Oncology, Dana Farber Cancer Institute, Boston, Massachusetts.
Abstract
BACKGROUND: ABO blood group has been associated with risk of cancers of the pancreas, stomach, ovary, kidney, and skin, but has not been evaluated in relation to risk of aggressive prostate cancer. METHODS: We used three single nucleotide polymorphisms (SNPs) (rs8176746, rs505922, and rs8176704) to determine ABO genotype in 2,774 aggressive prostate cancer cases and 4,443 controls from the Breast and Prostate Cancer Cohort Consortium (BPC3). Unconditional logistic regression was used to calculate age and study-adjusted odds ratios and 95% confidence intervals for the association between blood type, genotype, and risk of aggressive prostate cancer (Gleason score ≥8 or locally advanced/metastatic disease (stage T3/T4/N1/M1). RESULTS: We found no association between ABO blood type and risk of aggressive prostate cancer (Type A: OR = 0.97, 95%CI = 0.87-1.08; Type B: OR = 0.92, 95%CI =n0.77-1.09; Type AB: OR = 1.25, 95%CI = 0.98-1.59, compared to Type O, respectively). Similarly, there was no association between "dose" of A or B alleles and aggressive prostate cancer risk. CONCLUSIONS: ABO blood type was not associated with risk of aggressive prostate cancer.
BACKGROUND: ABO blood group has been associated with risk of cancers of the pancreas, stomach, ovary, kidney, and skin, but has not been evaluated in relation to risk of aggressive prostate cancer. METHODS: We used three single nucleotide polymorphisms (SNPs) (rs8176746, rs505922, and rs8176704) to determine ABO genotype in 2,774 aggressive prostate cancer cases and 4,443 controls from the Breast and Prostate Cancer Cohort Consortium (BPC3). Unconditional logistic regression was used to calculate age and study-adjusted odds ratios and 95% confidence intervals for the association between blood type, genotype, and risk of aggressive prostate cancer (Gleason score ≥8 or locally advanced/metastatic disease (stage T3/T4/N1/M1). RESULTS: We found no association between ABO blood type and risk of aggressive prostate cancer (Type A: OR = 0.97, 95%CI = 0.87-1.08; Type B: OR = 0.92, 95%CI =n0.77-1.09; Type AB: OR = 1.25, 95%CI = 0.98-1.59, compared to Type O, respectively). Similarly, there was no association between "dose" of A or B alleles and aggressive prostate cancer risk. CONCLUSIONS: ABO blood type was not associated with risk of aggressive prostate cancer.
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