Mutations in the adenomatous polyposis coli (APC) gene are the basis of fam
ilial adenomatous polyposis and the majority of sporadic colorectal cancer.
APC is expressed in a wide variety of tissues, interacts with the cytoskel
eton, is involved in regulating levels of beta -catenin and, most recently,
has been shown to bind DNA, suggesting that it may possess a nuclear role.
The mutation spectrum implicated in tumorigenesis and its correlation with
disease phenotype is well characterized and has contributed to our underst
anding of important functional domains in APC, Despite these advances, APC
continues to provide a fertile subject of research for both colorectal tumo
rigenesis and cancer in general.