Abstract: Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide. As with other cancers, CRC is a genetic disease, however, several risk factors including diet and chronic colitis predispose to the disease. Mutations in the tumor suppressor adenomatous polyposis coli (APC) initiate most cases of CRC. Recent data from mouse models suggest that APCmutations and colitis are not completely independent factors in colorectal carcinogenesis. Here, we review the evidence supporting an interaction between APC mutations and chronic colitis. We will also discuss possible pathophysiologic mechanisms behind this interaction.
Keywords: rodent model, colon cancer, adenomatous polyposis coli, APC, tumor suppressor, inflammatory bowel disease
Article first published: 30 January 2015
doi: http://dx.doi.org/10.2147/GICTT.S51386
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Citation: [Zeineldin M, Neufeld KL. New insights from animal models of colon cancer: inflammation control as a new facet on the tumor suppressor APC gem. Gastrointestinal Cancer: Targets and Therapy 2015:5 39–52]
Copyright: © 2015 Zeineldin and Neufeld. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/.
