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Iron overload may increase prostate cancer risk through stimulation of oxidative stress, and endogenous pro- and antioxidant capabilities, i.e. manganese superoxide dismutase (MnSOD) and myeloperoxidase (MPO), may modify these associations. We investigated this hypothesis in the Carotene and Retinol Efficacy Trial cohort in a nested case–control study. Although there was no association between iron intake and risk overall, there was a suggestion of increased risk of clinically aggressive prostate cancer with higher iron intake [odds ratio (OR) = 1.4, 95% confidence interval (CI) = 0.9–2.0]. Associations were most notable for men with aggressive prostate cancer who were below the median consumption of total fruits and vegetables (OR = 1.8, 95% CI = 1.1–3.2). Associations betweenMPO−463GtoAgenotype (rs2333227) and prostate cancer risk were only noted among men with aggressive cancer, with more than a 2-fold risk reduction among men withAAgenotypes (OR = 0.4, 95% CI = 0.2–1.0);MnSODwas not associated with risk overall, but theMnSOD TtoC(Val-9Ala, rs4880) polymorphism modified associations between risk of clinically aggressive prostate cancer and dietary iron intake (Pfor interaction = 0.02). Among aggressive cancer cases with theTTgenotype, higher iron intake level was associated with &gt;2-fold increase in risk (OR = 2.3, 95% CI = 1.0–4.9), whereas there was no association among men withCCgenotypes (OR = 0.9, 95% CI = 0.4–2.3). Although interactions were not significant, there were similar patterns forMPOgenotype, iron intake and risk. These findings suggest that higher iron intake may be associated with risk of clinically aggressive prostate cancer, and that endogenous antioxidant capabilities may modify these associations.

carcinogenesis

Iron intake, oxidative stress-related genes (              MnSOD               and               MPO              ) and prostate cancer risk in CARET cohort