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The effect of selenium on DNA methylation and gene expression in colon cancer

Colon cancer is a leading cause of death all over the world and its incidence is continuing to rise. Risk factors include age, family history and life style. The observation that colon cancer is markedly less in populations who follow a healthy diet rich in high fibre, fruit and vegetables has pointed to some clues towards diet and cancer preventions. Substances such as lycopenes found in fruit and vegetables, isoflavenoids, vitamin D and E, the mineral Se (found in Brazil nuts, offal and seafood) are currently being studied in trials. Of these substances, Se appears to be the most promising in contributing positively towards cancer prevention.

The anticancer action of Se has become increasingly recognized in both experimental animals and human trials. But the mechanisms through which Se and selenoproteins exert this effect are not fully clear.

Recent evidence suggests that low levels of certain selenoproteins may cause healthy human cells to transform to cancer cells. The levels of these selenoproteins have been found to depend on Se intake and on the type of selenoprotein their body makes. Individuals respond differently to dietary Se and this results from the particular variant form of the gene for the selenoprotein that they carry.

As well as inherited gene variants, non-inherited or ‘epigenetic’ modifications to genes can contribute to cancer risk. One of these epigenetic modifications is methylation of genes. In this study, I propose to analyse the way Se and gene methylation regulate selenoprotein and other genes thought to be involved in colon cancer.