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Differentiation of the Gastric Mucosa III. Animal models of oxyntic atrophy and metaplasia

¹Nashville Department of Veterans Affairs Medical Center and ²Department of Surgery and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; and ³Department of Gastrointestinal Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Submitted 2 May 2006 ; accepted in final form 15 May 2006

Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.

gastric adenocarcinoma; spasmolytic polypeptide-expressing metaplasia; trefoil factor 2; intestinal metaplasia

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