Carcinogenesis Advance Access originally published online on November 26, 2008
Carcinogenesis 2009 30(2):183-196; doi:10.1093/carcin/bgn267
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Mouse models for the study of colon carcinogenesis
Center for Molecular Medicine and Colon Cancer Prevention Program, Neag Cancer Center, University of Connecticut Health Center, Farmington, CT 06030-3101, USA
1 Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06113, USA
2 Department of Oncologic Pathology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-0293, Japan
* To whom correspondence should be addressed. Tel: +1 860 679 8704; Fax: +1 860 679 7639; Email: Rosenberg{at}uchc.edu
The study of experimental colon carcinogenesis in rodents has a long history, dating back almost 80 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 the pathogenesis of human colorectal cancer.
Abbreviations: AA, arachidonic acid; ACF, aberrant crypt foci; AOM, azoxymethane; Apc, adenomatous polyposis coli; BCAC, β-catenin-accumulated crypt; COX-2, cyclooxygenease-2; cPLA2, cytosolic phospholipase A2; CRC, colorectal cancer; DFMO, difluoromethylornithine; DMAB, 3,2'-dimethyl-4-aminobiphenyl; DMH, 1,2-dimethylhydrazine; DSS, dextran sodium sulfate; HCA, heterocyclic amine; IBD, inflammatory bowel disease; i.p., intraperitoneal; IQ, 2-amino-33-methylimidazo[4,5-f]quinoline; MAM, methylazoxymethanol; miRNA, microRNA; MNNG, N-methyl-N'-nitro-N-nitrosoguanidine; MNU, methylnitrosourea; ODC, ornithine decarboxylase; PGDH, 15-hydroxyprostaglandin dehydrogenase; PGE2, prostaglandin E2; PhIP, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine; s.c., subcutaneous; TGF, transforming growth factor; TNF, tumor necrosis factor
Received August 13, 2008; revised October 31, 2008; accepted November 20, 2008.
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