Carcinogenesis Advance Access published online on November 26, 2008
Carcinogenesis, doi:10.1093/carcin/bgn267
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Mouse models for the study of colon carcinogenesis
1 Center for Molecular Medicine, Colon Cancer Prevention Program, University of Connecticut Health Center, Farmington, CT 06030-3101
2 Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06113
3 Department of Oncologic Pathology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-0293, Japan
The study of experimental colon carcinogenesis in rodents has a long history, dating back almost eighty years. There are many advantages to studying the pathogenesis of carcinogen-induced colon cancer in mouse models, including rapid and reproducible tumor induction and the recapitulation of the adenoma-carcinoma sequence that occurs in humans. The availability of recombinant inbred mouse panels and the existence of transgenic, knock-out and knock-in genetic models further increase the value of these studies. In this review, we discuss the general mechanisms of tumor initiation elicited by commonly used chemical carcinogens and how genetic background influences the extent of disease. We will also describe the general features of lesions formed in response to carcinogen treatment, including the underlying molecular aberrations and how these changes may relate to human colorectal cancer.
Received August 13, 2008; revised October 31, 2008; accepted November 20, 2008.
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