Elimination of colon cancer in germ-free transforming growth factor beta 1-deficient mice

Sandra J. Engle, Ilona Ormsby, Sharon Pawlowski, Gregory P. Boivin, Joanne Croft, Edward Balish, Tom Doetschman

Research output: Contribution to journalArticlepeer-review

177 Scopus citations


Patients with ulcerative colitis are at risk for colon cancer and frequently have microsatellite instability, which, in turn, is usually associated with inactivation of transforming growth factor (TGF) β signaling. TGF-β1 deficiency in mice can lead to colon cancer that is preceded by precancerous lesions having submucosal inflammation and hyperplastic crypts. Germ-free TGF-β1-deficient mice are free of inflammation, hyperplasia, and cancer, but when reintroduced into a Helicobacter hepaticus-containing specific pathogen-free room, these lesions reappear. Because adenoma/carcinoma but not inflammation/hyperplasia is dependent on the genetic backgrounds tested, colitis is required, but not sufficient, for carcinogenesis. This animal model should provide insight into the protective role of TGF-β1 in early stages of ulcerative colitis-associated human colon cancer.

Original languageEnglish (US)
Pages (from-to)6362-6366
Number of pages5
JournalCancer Research
Issue number22
StatePublished - Nov 15 2002

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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