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There are few mouse models that adequately mimic large bowel cancer in humans or the gastrointestinal inflammation which frequently precedes it. Dextran sodium sulphate (DSS)-induces colitis in many animal models and has been used in combination with the carcinogen azoxymethane (AOM) to induce cancer in mice.  Smad3   −/−  mice are deficient in the transforming growth factor beta (TGFβ) signaling molecule,  SMAD3 , resulting in dysregulation of the cellular pathway most commonly affected in human colorectal cancer, and develop inflammation-associated colon cancer. Previous studies have shown a requirement for a bacterial trigger for the colitis and colon cancer phenotype in  Smad3 −/−   mice. Studies presented here in  Smad3 −/−   mice detail disease induction with DSS, without the use of AOM, and show a)  Smad3   −/−  mice develop a spectrum of lesions ranging from acute and chronic colitis, crypt herniation, repair, dysplasia, adenomatous polyps, disseminated peritoneal adenomucinosis, adenocarcinoma, mucinous adenocarcinoma (MAC) and squamous metaplasia; b) the colon lesions have variable galactin-3 (Mac2) staining c) increased DSS concentration and duration of exposure leads to increased severity of colonic lesions; d) heterozygosity of  SMAD3  does not confer increased susceptibility to DSS-induced disease and e) disease is partially controlled by the presence of T and B cells as  Smad3   −/−   Rag2   −/−  double knock out (DKO) mice develop a more severe disease phenotype. DSS-induced disease in  Smad3   −/−  mice may be a useful animal model to study not only inflammation-driven MAC but other human diseases such as colitis cystica profunda (CCP) and pseudomyxomatous peritonei (PMP).

Characterization of Dextran Sodium Sulfate-Induced Inflammation and Colonic Tumorigenesis in Smad3−/− Mice with Dysregulated TGFβ