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Gut 1998;43(Supplement 1):S27-S32; doi:10.1136/gut.43.2008.S27
Copyright © 1998 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 1998;43(Suppl 1):S27-S32 ( July )

Importance of changes in epithelial cell turnover during Helicobacter pylori infection in gastric carcinogenesis

M Antia, A Armuzzia, A Gasbarrinib, G Gasbarrinia

a Cattedra di Medicina Interna II, Università Cattolica del Sacro Cuore, Largo F. Vito 1, 00168 Rome, Italy, b Istituto di Patologia Medica, Università Cattolica del Sacro Cuore, Rome, Italy

Correspondence to: Dr Anti.

The first 150 words of the full text of this article appear below.

    Summary

The role of Helicobacter pylori in gastric carcinogenesis is supported almost exclusively by epidemiological data and prospective histopathological studies. From biological and molecular points of view, there is no evidence that H pylori or its cytotoxic products have any mutagenic effects. Nevertheless, this infection is associated with profound changes in the pattern of epithelial cell turnover in gastric glands, though the importance of these changes in gastric carcinogenesis is still controversial. H pylori infection increases cell proliferation and alters the distribution of cycling cells within these glands, but these changes can be reversed by successful eradication of the infection. Apoptosis seems to be increased in gastric epithelial cells during H pylori infection, as shown by in vitro studies. There is some, though no conclusive, evidence that this finding also occurs in H pylori positive subjects. It seems that cagA status influences the effect of H pylori on epithelial apoptosis in . . . [Full text of this article]


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