Colon cancer and nutrigenetics: modifier genes

About 5% of colon cancer cases correspond to classic hereditary monogenic m endelian transmission involving at least 8 major genes of predisposition to this tumor. Genes with more moderate effects, in association with other ge nes can contribute to the occurrence of sporadic polygenic forms. These gen es confer susceptibility to environmental factors and can play the role of aggravating or protective modifier genes in the different hereditary forms. Foods can interact with these genes and modulate their expression. Moreove r sequence variations (polymorphisms) in these genes may also be responsibl e for slower or more rapid metabolism of nutrients leading to toxic or carc inogenic compounds. If some foods, or "pharmafoods" can have beneficial eff ects in some individuals with a particular subtype of the disease, others c an be inefficient or even detrimental in patients with the same disease but with a different genetic origin or if the genetic background is different. Moreover tumorigenic processes are diverse. Tumor progression depends on g enetic and environnemental factors different from tumor initiation and on t he site of the tumor along the colon tract. Interactions with the gut flora , the lymphoid system and specific features of growth of the colon mucosa a re also important parameters. Today with a formidable genetic knowledge ari sing from the genome project, new epidemiological data integrating the gene tic data for multiple markers and a better knowledge of the tumorigenic pro cesses involved, a new discipline is emerging. "Nutrigenetics" which is the study of hereditary basis of individual variations in response to foods op ens for the oncoming decade the era of a personnalised predictive medecine based on a nutrition adapted to the genetic make up of each of us.