Animal Models of Colitis-Associated Carcinogenesis

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 fo...

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Main Authors: Manasa Kanneganti, Mari Mino-Kenudson, Emiko Mizoguchi
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Journal of Biomedicine and Biotechnology
Online Access:http://dx.doi.org/10.1155/2011/342637
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spelling doaj-460f17a2659f43a1a971d285b28bff812020-11-25T02:15:04ZengHindawi LimitedJournal of Biomedicine and Biotechnology1110-72431110-72512011-01-01201110.1155/2011/342637342637Animal Models of Colitis-Associated CarcinogenesisManasa Kanneganti0Mari Mino-Kenudson1Emiko Mizoguchi2Gastrointestinal Unit, Department of Medicine, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USADepartment of Pathology, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USAGastrointestinal Unit, Department of Medicine, Harvard Medical School, Massachusetts General Hospital, GRJ 702, 55 Fruit Street, Boston, MA 02114, USAInflammatory 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.http://dx.doi.org/10.1155/2011/342637
collection DOAJ
language English
format Article
sources DOAJ
author Manasa Kanneganti
Mari Mino-Kenudson
Emiko Mizoguchi
spellingShingle Manasa Kanneganti
Mari Mino-Kenudson
Emiko Mizoguchi
Animal Models of Colitis-Associated Carcinogenesis
Journal of Biomedicine and Biotechnology
author_facet Manasa Kanneganti
Mari Mino-Kenudson
Emiko Mizoguchi
author_sort Manasa Kanneganti
title Animal Models of Colitis-Associated Carcinogenesis
title_short Animal Models of Colitis-Associated Carcinogenesis
title_full Animal Models of Colitis-Associated Carcinogenesis
title_fullStr Animal Models of Colitis-Associated Carcinogenesis
title_full_unstemmed Animal Models of Colitis-Associated Carcinogenesis
title_sort animal models of colitis-associated carcinogenesis
publisher Hindawi Limited
series Journal of Biomedicine and Biotechnology
issn 1110-7243
1110-7251
publishDate 2011-01-01
description 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.
url http://dx.doi.org/10.1155/2011/342637
work_keys_str_mv AT manasakanneganti animalmodelsofcolitisassociatedcarcinogenesis
AT mariminokenudson animalmodelsofcolitisassociatedcarcinogenesis
AT emikomizoguchi animalmodelsofcolitisassociatedcarcinogenesis
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