ABSTRACT
In humans, adequate dietary selenium intake is essential for synthesizing 25 selenoproteins, of which several are important in countering oxidative and inflammatory processes linked to carcinogenesis. Experimental and observational studies suggest that suboptimal selenium intake, as found across Europe, for example, and genetic variations in several selenoprotein genes may contribute to cancer development, particularly at gastrointestinal anatomical sites. Pathway analyses indicated that for genes in antioxidant/redox and apoptotic pathways the influence of single nucleotide polymorphisms (SNPs) on the disease risk is also dependent on interaction with selenium status. Multivariable odds ratios and 95% confidence intervals were calculated using logistic regression to determine the association of selenium status biomarkers with cancer risk and of SNPs in the selenium pathway with colorectal cancer risk. Detailed investigation of selenium intake levels and metabolism is needed to more fully elucidate the relevance for cancer etio-pathogenesis, especially for populations with diverse selenium status levels and/or individuals with potentially at-risk or cancer protective selenium pathway genotypes.
