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The role of mutant apc in the development of dysplasia and cancer in the mouse model of dextran sulfate sodium-induced colitis
Journal article   Open access   Peer reviewed

The role of mutant apc in the development of dysplasia and cancer in the mouse model of dextran sulfate sodium-induced colitis

Harry S. Cooper, Lynette Everley, Wen-Chi Chang, Gordon Pfeiffer, Bryan Lee, Sreekant Murthy and Margie L. Clapper
Gastroenterology (New York, N.Y. 1943), v 121(6), pp 1407-1416
Dec 2001
DOI: https://doi.org/10.1053/gast.2001.29609
PMID: 11729120
Featured in Collection :   UN Sustainable Development Goals @ Drexel
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https://doi.org/10.1053/gast.2001.29609View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

CTT IS LOH DSS US
Differences in genetic background may play a role in the development of ulcerative colitis (UC)-related neoplasia. Loss of heterozygosity (LOH) of APC has been reported in human UC-associated neoplasia. To investigate the role of genetic differences in UC-associated neoplasia, we compared differences in dextran sodium sulfate (DSS) colitis-associated neoplasia between wild-type C57BL/6J mice (WT-DSS) and C57BL/6J mice with a germline mutation in Apc (Min-DSS). DSS colitis was induced in female wildtype and Min mice. Age- and sex-matched non-DSS-treated Mins were also studied. Animals were sacrificed after 1 and 2 cycles of DSS. The cecums and large intestines were studied for numbers of dysplasias/cancers. Dysplasias were studied for LOH of Apc. No WT-DSS, 100% of Min-DSS, and 50% of non-DSS-treated Mins had dysplasia. The mean numbers of lesions per mouse were 0 (WT-DSS), 15.6 and 29.3 (1 and 2 cycles Min-DSS, respectively), 1.2 and 1.9 (age-matched control Min, 1 and 2 cycle equivalents, respectively; P < 0.0002, Min-DSS vs. WT-DSS and non-DSS-treated Min; P = 0.03, Min-DSS 2 cycle vs. Min-DSS 1 cycle). Cancers were seen in 0%, 22%, and 40% of non-DSS Min, Min-DSS-1 cycle, and Min-DSS-2 cycle animals, respectively. LOH of Apc was observed in 90.6% of dysplasias and 6% of nondysplastic mucosa. A germline mutation in Apc contributes significantly to the development of colitis-associated neoplasia. Colitis markedly accelerates the development of dysplasia and cancer in the Min mouse. Dysplasia in Min-DSS occurs through LOH of Apc.

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Collaboration types
Domestic collaboration
Web of Science research areas
Gastroenterology & Hepatology
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