Timothy J Key1, Paul N Appleby2, Ruth C Travis2, Demetrius Albanes3, Anthony J Alberg4, Aurelio Barricarte5, Amanda Black3, Heiner Boeing6, H Bas Bueno-de-Mesquita7, June M Chan8, Chu Chen9, Michael B Cook3, Jenny L Donovan10, Pilar Galan11, Rebecca Gilbert10, Graham G Giles12, Edward Giovannucci13, Gary E Goodman14, Phyllis J Goodman15, Marc J Gunter16, Freddie C Hamdy17, Markku Heliövaara18, Kathy J Helzlsouer19, Brian E Henderson20, Serge Hercberg11, Judy Hoffman-Bolton21, Robert N Hoover3, Mattias Johansson22, Kay-Tee Khaw23, Irena B King24, Paul Knekt18, Laurence N Kolonel25, Loic Le Marchand25, Satu Männistö18, Richard M Martin26, Haakon E Meyer27, Alison M Mondul3, Kristin A Moy3, David E Neal28, Marian L Neuhouser29, Domenico Palli30, Elizabeth A Platz31, Camille Pouchieu12, Harri Rissanen18, Jeannette M Schenk32, Gianluca Severi12, Meir J Stampfer13, Anne Tjønneland33, Mathilde Touvier11, Antonia Trichopoulou34, Stephanie J Weinstein3, Regina G Ziegler3, Cindy Ke Zhou3, Naomi E Allen35. 1. Cancer Epidemiology Unit, Nuffield Department of Population Health, tim.key@ceu.ox.ac.uk. 2. Cancer Epidemiology Unit, Nuffield Department of Population Health. 3. Division of Cancer Epidemiology and Genetics, US National Cancer Institute, Bethesda, MD; 4. Department of Epidemiology, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD; Hollings Cancer Center, Medical University of South Carolina, Charleston, SC; 5. Navarre Public Health Institute, Pamplona, Spain, and Consortium for Biomedical Research in Epidemiology and Public Health (CIBER Epidemiología y Salud Pública), Spain; 6. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany; 7. National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands; Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, Netherlands; School of Public Health, Imperial College, London, United Kingdom; 8. Departments of Epidemiology & Biostatistics and Urology, University of California, San Francisco, San Francisco, CA; 9. Public Health Sciences Division, Program in Epidemiology. 10. School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom; 11. Sorbonne Paris Cité Epidemiology and Biostatistics Research Center, Nutritional Epidemiology Research Team (Nutritional Epidemiology Research Team), Inserm U1153, Inra U1125, Cnam, University Paris 13, University Paris 5, University Paris 7, Bobigny, France; 12. Cancer Epidemiology Centre, The Cancer Council Victoria, Melbourne, Australia; 13. Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; 14. Departments of Epidemiology and Environmental Health, University of Washington, Seattle, WA; 15. SWOG Statistical Center. 16. School of Public Health, Imperial College, London, United Kingdom; 17. Department of Surgery, and. 18. National Institute for Health and Welfare, Helsinki, Finland; 19. Prevention and Research Center Mercy Medical Center, Baltimore, MD; 20. Keck School of Medicine, University of Southern California, Los Angeles, CA; 21. George W Comstock Center for Public Health Research and Prevention, Hagerstown, MD; 22. International Agency for Research on Cancer, Lyon, France; Department for Biobank Research, Umeå University, Umeå, Sweden; 23. Department of Public Health and Primary Care and. 24. Public Health Sciences Core Laboratories, Department of Internal Medicine, University of New Mexico, Albuquerque, NM. 25. University of Hawaii Cancer Center, Honolulu, HI; 26. School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom; Medical Research Council/University of Bristol Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom; National Institute for Health Research, Bristol Biomedical Research Unit in Nutrition, Bristol, United Kingdom; 27. Department of Community Medicine, Faculty of Medicine, University of Oslo and Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway; 28. Department of Oncology, University of Cambridge, Cambridge, United Kingdom; 29. Division of Public Health Sciences, and. 30. Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute-ISPO, Florence, Italy; 31. Department of Epidemiology, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD; 32. Cancer Prevention Program, Fred Hutchinson Cancer Research Center, Seattle, WA; 33. Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark; 34. Hellenic Health Foundation and Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece and. 35. Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom;
Abstract
BACKGROUND: Individual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease. OBJECTIVE: The objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors. DESIGN: Principal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets. RESULTS: Data were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For α-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). γ-Tocopherol was not associated with risk. CONCLUSIONS: Overall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.
BACKGROUND: Individual studies have suggested that circulating carotenoids, retinol, or tocopherols may be associated with prostate cancer risk, but the studies have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease. OBJECTIVE: The objective of this study was to conduct a pooled analysis of the associations of the concentrations of 7 carotenoids, retinol, α-tocopherol, and γ-tocopherol with risk of prostate cancer and to describe whether any associations differ by stage or grade of the disease or other factors. DESIGN: Principal investigators of prospective studies provided individual participant data for prostate cancer cases and controls. Risk by study-specific fifths of each biomarker was estimated by using multivariable-adjusted conditional logistic regression in matched case-control sets. RESULTS: Data were available for up to 11,239 cases (including 1654 advanced stage and 1741 aggressive) and 18,541 controls from 15 studies. Lycopene was not associated with overall risk of prostate cancer, but there was statistically significant heterogeneity by stage of disease, and the OR for aggressive disease for the highest compared with the lowest fifth of lycopene was 0.65 (95% CI: 0.46, 0.91; P-trend = 0.032). No other carotenoid was significantly associated with overall risk of prostate cancer or with risk of advanced-stage or aggressive disease. For retinol, the OR for the highest compared with the lowest fifth was 1.13 (95% CI: 1.04, 1.22; P-trend = 0.015). For α-tocopherol, the OR for the highest compared with the lowest fifth was 0.86 (95% CI: 0.78, 0.94; P-trend < 0.001), with significant heterogeneity by stage of disease; the OR for aggressive prostate cancer was 0.74 (95% CI: 0.59, 0.92; P-trend = 0.001). γ-Tocopherol was not associated with risk. CONCLUSIONS: Overall prostate cancer risk was positively associated with retinol and inversely associated with α-tocopherol, and risk of aggressive prostate cancer was inversely associated with lycopene and α-tocopherol. Whether these associations reflect causal relations is unclear.
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