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(American Journal of Pathology. 2009;175:365-375.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.081165

Gastrin Is an Essential Cofactor for Helicobacter-Associated Gastric Corpus Carcinogenesis in C57BL/6 Mice

Shigeo Takaishi*, Shuiping Tu*, Zinaida A. Dubeykovskaya*, Mark T. Whary{dagger}, Sureshkumar Muthupalani{dagger}, Barry H. Rickman{dagger}, Arlin B. Rogers{dagger}, Nantaporn Lertkowit{ddagger}, Andrea Varro{ddagger}, James G. Fox{dagger} and Timothy C. Wang*

From the Division of Digestive and Liver Disease,* Department of Medicine, Columbia University Medical Center, New York, New York; the Division of Comparative Medicine,{dagger} Massachusetts Institute of Technology, Cambridge, Massachusetts; and the Physiological Laboratory,{ddagger} School of Biomedical Sciences, University of Liverpool, Liverpool, United Kingdom

We have previously described a synergistic interaction between hypergastrinemia and Helicobacter felis infection on gastric corpus carcinogenesis in FVB/N mice housed under specific-pathogen-free conditions. However, gastrin-deficient (GAS-KO) mice on a mixed C57BL/6/129Sv genetic background maintained in conventional housing were reported to develop spontaneous gastric antral tumors. Therefore, we investigated the role of gastrin in Helicobacter-associated gastric carcinogenesis in H. felis-infected mice on a uniform C57BL/6 background housed in specific-pathogen-free conditions. Hypergastrinemic transgenic (INS-GAS) mice, GAS-KO mice, and C57BL/6 wild-type mice were infected with H. felis for either 12 or 18 months. At 12 months postinfection, INS-GAS mice had mild corpus dysplasia, while B6 wild-type mice had either severe gastritis or metaplasia, and GAS-KO mice had only mild to moderate gastritis. At 18 months postinfection, both INS-GAS and B6 wild-type mice had both severe atrophic gastritis and corpus dysplasia, while GAS-KO mice had severe gastritis with mild gastric atrophy, but no corpus dysplasia. In contrast, both GAS-KO and B6 wild-type mice had mild to moderate antral dysplasia, while INS-GAS mice did not. H. felis antral colonization remained stable over time among the three groups of mice. These results point to a distinct effect of gastrin on carcinogenesis of both the gastric corpus and antrum, suggesting that gastrin is an essential cofactor for gastric corpus carcinogenesis in C57BL/6 mice.


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