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Investigating the possible causal role of coffee consumption with prostate cancer risk and progression using Mendelian randomization analysis.
Pubmed ID
27741566 (View this publication on the PubMed website)
Int. J. Cancer. 2017 Jan; Volume 140 (Issue 2): Pages 322-328
Taylor AE, Martin RM, Geybels MS, Stanford JL, Shui I, Eeles R, Easton D, Kote-Jarai Z, Amin Al Olama A, Benlloch S, Muir K, Giles GG, Wiklund F, Gronberg H, Haiman CA, Schleutker J, Nordestgaard BG, Travis RC, Neal D, Pashayan N, more Khaw KT, Blot W, Thibodeau S, Maier C, Kibel AS, Cybulski C, Cannon-Albright L, Brenner H, Park J, Kaneva R, Batra J, Teixeira MR, Pandha H, PRACTICAL Consortium, Donovan J, Munafò MR
  • MRC Integrative Epidemiology Unit (IEU) at the University of Bristol, Bristol, United Kingdom.
  • Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA.
  • The Institute of Cancer Research, London, SM2 5NG, United Kingdom.
  • Strangeways Laboratory, Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Worts Causeway, Cambridge, United Kingdom.
  • Institute of Population Health, University of Manchester, Manchester, United Kingdom.
  • Cancer Epidemiology Centre, Cancer Council Victoria, 615 St Kilda Road, Melbourne, VIC, Australia.
  • Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
  • Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, CA.
  • Department of Medical Biochemistry and Genetics, University of Turku, Turku, Finland.
  • Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev Ringvej 75, Herlev, 2730, Denmark. more
  • Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom.
  • Surgical Oncology (Uro-Oncology: S4), University of Cambridge, Addenbrooke's Hospital, Hills Road, Box 279, Cambridge, United Kingdom.
  • Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, VIC, Australia.
  • Cambridge Institute of Public Health, University of Cambridge, Forvie Site, Robinson Way, Cambridge, CB2 0SR, United Kingdom.
  • International Epidemiology Institute, 1455 Research Blvd, Suite 550, Rockville, MD.
  • Mayo Clinic, Rochester, MN.
  • Department of Urology, University Hospital Ulm, Ulm, Germany.
  • Brigham and Women's Hospital/Dana-Farber Cancer Institute, 45 Francis Street-ASB II-3, Boston, MA.
  • International Hereditary Cancer Center, Department of Genetics and Pathology, Pomeranian Medical University, Szczecin, Poland.
  • Division of Genetic Epidemiology, Department of Medicine, University of Utah School of Medicine, Salt Lake City, UT.
  • Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • Division of Cancer Prevention and Control, H. Lee Moffitt Cancer Center, 12902 Magnolia Dr, Tampa, FL.
  • Molecular Medicine Center and Department of Medical Chemistry and Biochemistry, Medical University Sofia, 2 Zdrave St, Sofia, 1431, Bulgaria.
  • Australian Prostate Cancer Research Centre-Qld, Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Brisbane, QLD, Australia.
  • Department of Genetics, Portuguese Oncology Institute, Porto, Portugal.
  • Faculty of Health & Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, United Kingdom.
  • School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.

Coffee consumption has been shown in some studies to be associated with lower risk of prostate cancer. However, it is unclear if this association is causal or due to confounding or reverse causality. We conducted a Mendelian randomisation analysis to investigate the causal effects of coffee consumption on prostate cancer risk and progression. We used two genetic variants robustly associated with caffeine intake (rs4410790 and rs2472297) as proxies for coffee consumption in a sample of 46,687 men of European ancestry from 25 studies in the PRACTICAL consortium. Associations between genetic variants and prostate cancer case status, stage and grade were assessed by logistic regression and with all-cause and prostate cancer-specific mortality using Cox proportional hazards regression. There was no clear evidence that a genetic risk score combining rs4410790 and rs2472297 was associated with prostate cancer risk (OR per additional coffee increasing allele: 1.01, 95% CI: 0.98,1.03) or having high-grade compared to low-grade disease (OR: 1.01, 95% CI: 0.97,1.04). There was some evidence that the genetic risk score was associated with higher odds of having nonlocalised compared to localised stage disease (OR: 1.03, 95% CI: 1.01, 1.06). Amongst men with prostate cancer, there was no clear association between the genetic risk score and all-cause mortality (HR: 1.00, 95% CI: 0.97,1.04) or prostate cancer-specific mortality (HR: 1.03, 95% CI: 0.98,1.08). These results, which should have less bias from confounding than observational estimates, are not consistent with a substantial effect of coffee consumption on reducing prostate cancer incidence or progression.

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