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Cancer Prev Res (Phila). 2014 Sep;7(9):886-95. doi: 10.1158/1940-6207.CAPR-14-0058. Epub 2014 Jun 24.

Plasma tocopherols and risk of prostate cancer in the Selenium and Vitamin E Cancer Prevention Trial (SELECT).

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Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Department of Urology, Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, Ohio.
Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland.
Massachusetts Veteran's Epidemiology, Research and Information Center, VA Boston Healthcare System, Boston, Massachusetts.
Biomarker Laboratory, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Princess Margaret Hospital, University of Toronto, Toronto, Ontario, Canada.
The University of Texas MD Anderson Cancer Center, Houston, Texas.
University of California at Irvine, Department of Medicine, Orange, California.
Cancer Therapy and Research Center, University of Texas Health Science Center, San Antonio, Texas.


The Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed higher prostate cancer incidence in men supplemented with high-dose α-tocopherol. We, therefore, examined whether presupplementation plasma α-tocopherol or γ-tocopherol was associated with overall or high-grade prostate cancer. A stratified case-cohort sample that included 1,746 incident prostate cancer cases diagnosed through June 2009 and a subcohort of 3,211 men was derived from the SELECT trial of 35,533 men. Plasma was collected at entry from 2001 to 2004, and median follow-up was 5.5 years (range, 0-7.9 years). Incidence of prostate cancer as a function of plasma α-tocopherol, γ-tocopherol, and supplementation with α-tocopherol or selenomethionine was estimated by the hazard ratio (HR). Plasma γ-tocopherol was not associated with prostate cancer. Men with higher α-tocopherol concentrations seemed to have risk similar to that of men with lower concentrations [overall HR for fifth (Q5) vs. first quintile (Q1), 1.21; 95 % confidence interval (CI), 0.88-1.66; P-trend = 0.24; in the trial placebo arm, Q5 HR, 0.85; 95% CI, 0.44-1.62; P-trend = 0.66]. We found a strong positive plasma α-tocopherol association among men receiving the trial selenomethionine supplement [Q5 HR, 2.04; 95% CI, 1.29-3.22; P-trend = 0.005]. A positive plasma α-tocopherol-prostate cancer association also seemed limited to high-grade disease (Gleason grade, 7-10; overall Q5 HR, 1.59; 95% CI, 1.13-2.24; P-trend = 0.001; among men receiving selenomethionine, Q5 HR, 2.12; 95% CI, 1.32-3.40; P-trend = 0.0002). Our findings indicate that higher plasma α-tocopherol concentrations may interact with selenomethionine supplements to increase high-grade prostate cancer risk, suggesting a biologic interaction between α-tocopherol and selenium itself or selenomethionine.

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