Cancer in inflammatory bowel disease: Lessons from animal models

Daniel A. Sussman, Rebeca Santaolalla, Sebastian Strobel, Rishu Dheer, Maria T. Abreu

Research output: Contribution to journalReview articlepeer-review

34 Scopus citations


Purpose of review: Human colitis-associated cancers (CAC) represent a heterogeneous group of conditions in which multiple oncogenic pathways are involved. In this article, we review the latest studies using genetic, chemical, bacterial and innate immune-mediated experimental models of CAC. Recent findings: Using the azoxymethane-dextran sodium sulfate model, wound healing pathways seem to be required in the development of CAC. There is also an emerging understanding that commensal and/or pathogenic bacteria can promote tumorigenesis, through T cell and TLR-mediated inflammation. Using specific transgenic mice (villin-CD98, T cell SMAD7, villin-TLR4) or specific knockout mice, investigators have determined that derangements in epithelial or innate and adaptive immune pathways can result in CAC. Subtle perturbations in epithelial repair - both too little or too exuberant - can render mice susceptible to tumorigenesis. Summary: With the aid of animal models, we have witnessed a rapid expansion of our knowledge of the molecular and immunologic mechanisms underlying inflammatory cancers. Though animal models have contributed a discrete amount of information to our understanding of tumorigenesis in the setting of intestinal inflammation, it is clear that no single animal model will be able to adequately recapitulate the pathogenesis of complex colorectal cancers, but each model gets us one step closer to comprehending the nature of CAC.

Original languageEnglish (US)
Pages (from-to)327-333
Number of pages7
JournalCurrent opinion in gastroenterology
Issue number4
StatePublished - Jul 2012


  • adenomatous polyposis coli
  • azoxymethane
  • colitis cancer
  • dextran sodium sulfate
  • mouse

ASJC Scopus subject areas

  • Gastroenterology


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