Gastric Mucosa Abnormalities and Tumorigenesis in Mice Lacking the pS2 Trefoil Protein
Olivier Lefèbvre(Centre National de la Recherche Scientifique), Marie‐Pierre Chenard(Hôpital d'Hautepierre), Régis Masson(Centre National de la Recherche Scientifique), José Luis Linares(Centre National de la Recherche Scientifique), Andrée Dierich(Centre National de la Recherche Scientifique), Marianne LeMeur(Centre National de la Recherche Scientifique), Corinne Wendling(Centre National de la Recherche Scientifique), Catherine Tomasetto(Centre National de la Recherche Scientifique), Pierre Chambon(Centre National de la Recherche Scientifique), Marie–Christine Rio(Centre National de la Recherche Scientifique)
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Abstract
To determine the function of the pS2 trefoil protein, which is normally expressed in the gastric mucosa, the mouse pS2 (mpS2) gene was inactivated. The antral and pyloric gastric mucosa of mpS2-null mice was dysfunctional and exhibited severe hyperplasia and dysplasia. All homozygous mutant mice developed antropyloric adenoma, and 30 percent developed multifocal intraepithelial or intramucosal carcinomas. The small intestine was characterized by enlarged villi and an abnormal infiltrate of lymphoid cells. These results indicate that mpS2 is essential for normal differentiation of the antral and pyloric gastric mucosa and may function as a gastric-specific tumor suppressor gene.
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