Edited by
Inke S. Niithke
Brooke M. McCartney

2009

The initial identification of the Adenomatous polyposis coli (Apc) gene as the site of mutations in familial adenomatous polyposis (FAP) was described in 1992. A causal relationship between Apc mutations and intestinal tract tumours was confirmed three years later with the establishment of the Min mouse model. These mice are heterozygous for Apc and develop numerous intestinal tumours that mimic FAP. Subsequently, Apc has emerged as the most commonly mutated gene in colorectal cancer with reports varying between 50-80% of sporadic tumours carrying such mutations.