About this Journal Submit a Manuscript Table of Contents
Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 342637, 23 pages
http://dx.doi.org/10.1155/2011/342637
Research Article

Animal Models of Colitis-Associated Carcinogenesis

1Gastrointestinal Unit, Department of Medicine, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USA
2Department of Pathology, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USA
3Center for the Study of Inflammatory Bowel Disease, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USA

Received 27 September 2010; Revised 8 December 2010; Accepted 10 December 2010

Academic Editor: Andrea Vecchione

Copyright © 2011 Manasa Kanneganti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders that affect individuals throughout life. Although the etiology and pathogenesis of IBD are largely unknown, studies with animal models of colitis indicate that dysregulation of host/microbial interactions are requisite for the development of IBD. Patients with long-standing IBD have an increased risk for developing colitis-associated cancer (CAC), especially 10 years after the initial diagnosis of colitis, although the absolute number of CAC cases is relatively small. The cancer risk seems to be not directly related to disease activity, but is related to disease duration/extent, complication of primary sclerosing cholangitis, and family history of colon cancer. In particular, high levels and continuous production of inflammatory mediators, including cytokines and chemokines, by colonic epithelial cells (CECs) and immune cells in lamina propria may be strongly associated with the pathogenesis of CAC. In this article, we have summarized animal models of CAC and have reviewed the cellular and molecular mechanisms underlining the development of carcinogenic changes in CECs secondary to the chronic inflammatory conditions in the intestine. It may provide us some clues in developing a new class of therapeutic agents for the treatment of IBD and CAC in the near future.