Apc mice: models, modifiers and mutants

Pathol Res Pract. 2008;204(7):479-90. doi: 10.1016/j.prp.2008.03.004. Epub 2008 Jun 5.


The mouse provides an excellent in vivo system with which to model human diseases and to test therapies. Mutations in the Adenomatous polyposis coli (APC) gene are required to initiate familial adenomatous polyposis (FAP) and are also important in sporadic colorectal cancer tumorigenesis. The (multiple intestinal neoplasia Min) mouse contains a point mutation in the Apc gene, develops numerous adenomas and was the first model used to study the involvement of the Apc gene in intestinal tumorigenesis. The model has provided examples of modifying loci (called Modifiers of Min: Mom) in mice, demonstrating the principle of genetic modulation of disease severity. A spectrum of Apc mutant mice has since been developed, each with defining characteristics, some more able to accurately model human polyposis and colon cancer. We will focus our review on Apc mutant mouse models, the advent of models with concurrent or compound mutations and the importance of genetic background when modeling polyposis and cancer. Brief consideration will be given to the use of these models in drug testing.

Publication types

  • Review

MeSH terms

  • Adenomatous Polyposis Coli / drug therapy
  • Adenomatous Polyposis Coli / genetics*
  • Adenomatous Polyposis Coli / pathology
  • Animals
  • Colorectal Neoplasms / drug therapy
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / pathology
  • Disease Models, Animal*
  • Drug Screening Assays, Antitumor
  • Gene Expression Regulation, Neoplastic
  • Genes, APC*
  • Genomic Instability
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains