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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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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