Mouse models for colorectal cancer

Joerg Heyer, Kan Yang, Martin Lipkin, Winfried Edelmann, Raju Kucherlapati

Research output: Contribution to journalReview articlepeer-review

63 Scopus citations


Colorectal cancer (CRC) is one of the most common cancers in the Western world. Much has been learned about colorectal cancer from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). Mouse models for CRC were generated by introducing mutations into the mouse genes, whose human counterparts were implicated in the onset and progression of CRC. Central among these are mice carrying mutations in the Adenomatous polyposis coli (Apc) gene. Although most of these Apc mutations share some common phenotypes as homozygous embryonic lethality and tumor predisposition, the severity of the tumor predisposition is variable. Mice with mutations in the mismatch repair genes, Msh2 and Mlh1, exhibit a mismatch repair defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other organ systems. Mice carrying a mutation in the Pms2 gene are predisposed to lymphomas and other tumors. Mice with a mutation in the Msh6 gene have a defect in base mismatch repair and show a tumor predisposition phenotype. Mice with mutations in Mlh1, Pms2 and Msh5 have defects in meiosis suggesting unique roles for these genes in gametogenesis.

Original languageEnglish (US)
Pages (from-to)5325-5333
Number of pages9
Issue number38
StatePublished - Sep 20 1999


  • FAP
  • Gastrointestinal cancer
  • Mouse

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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