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[Cancer Research 62, 6362-6366, November 15, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Elimination of Colon Cancer in Germ-free Transforming Growth Factor Beta 1-deficient Mice1

Sandra J. Engle, Ilona Ormsby, Sharon Pawlowski, Gregory P. Boivin, Joanne Croft, Edward Balish and Tom Doetschman2

Departments of Molecular Genetics, Biochemistry and Microbiology [S. J. E., I. O., S. P., T. D.] and Comparative Pathology [G. P. B.], University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524; Aventis Pharmaceuticals, Bridgewater, New Jersey 08807 [S. J. E.]; Department of Surgery, University of Wisconsin Medical School, Madison, Wisconsin 53706-1087 [J. C., E. B.]; and Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, South Carolina 29425 [E. B.]

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) ß signaling. TGF-ß1 deficiency in mice can lead to colon cancer that is preceded by precancerous lesions having submucosal inflammation and hyperplastic crypts. Germ-free TGF-ß1-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-ß1 in early stages of ulcerative colitis-associated human colon cancer.




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Copyright © 2002 by the American Association for Cancer Research.