Colon polyps: a damaged developmental system and a precursor to cancer.
The observation that the attenuated form of adenomatous polyposis coli (AAPC) has a different mutational spectrum in both the adenomatous polyp and the carcinoma than the classical form of APC has led to the hypothesis that AAPC alleles retain some residual APC activity associated with a greatly reduced number of polyps. It is suggested that further progression to carcinoma may be dependent upon either loss of the AAPC allele (loss of heterozygosity), followed by an APC mutation in the wild-type allele, or the occurrence of APC mutations within both the AAPC and wild-type alleles.
White
R L
RL
Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. ray.white@hci.utah.edu
D011125:Adenomatous Polyposis Coli / Q000235:genetics / Q000473:pathology; D025601:Adenomatous Polyposis Coli Protein; D002467:Cell Nucleus / Q000378:metabolism; D003111:Colonic Polyps / Q000235:genetics* / Q000473:pathology*; D003598:Cytoskeletal Proteins / Q000235:genetics / Q000378:metabolism; D017491:Genes, APC / Q000235:genetics / Q000502:physiology; D014644:Genetic Variation / Q000235:genetics; D006801:Humans; D019656:Loss of Heterozygosity / Q000235:genetics; D009154:Mutation / Q000235:genetics; D011230:Precancerous Conditions / Q000235:genetics* / Q000473:pathology*; D011485:Protein Binding
D025601:Adenomatous Polyposis Coli Protein; D003598:Cytoskeletal Proteins