Modulation by dietary factors in murine FAP models.
Germline mutations of the tumor suppressor gene adenomateous polyposis coli (APC) lead to familial adenomatous polyposis (FAP) characterised by the development of multiple colorectal adenomas. In both FAP, murine FAP models and the majority of human sporadic colorectal cancers, tumour initiation seems to be dependent on somatic genetic events that lead to the inactivation of both APC alleles. Murine FAP strains are excellent models for studying the influence of environmental factors on critical events in Apc-driven tumourigenesis, since they select for factors that disrupt the Apc gene or factors that compensate for lost Apc function.