Background & Objective: Helicobacter pylori (Hp) are believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. p53, p21WAF1, and p16 are main negative regulator genes of cell cycle. This study was designed to investigate the relationship between these 3 genes and Hp infection.

Methods: The authors examined the expression of these 3 tumor suppressor genes and Hp infection in 65 cases with chronic atrophic gastritis (CAG), 93 cases with intestinal metaplasia(IM), 94 cases with gastric epithelial dysplasia (GED) and 60 cases with gastric carcinoma (GC) using HID-AB (pH 2.5)-PAS, SP immunohistochemistry staining, and Warthin-Starry staining.

Results: For CAC, IM stage I-II, IM stage III, GED stage I, GED stage II-III, and GC, the positive expression rates of p53 were 0, 1.64%, 6.25%, 5.45%, 23.08%, and 70.00%, respectively (increased with pathological process); the positive expression rates of p21WAF1 were 100%, 95.08%, 100%, 100%, 71.79%, and 45.00%, respectively; the positive expression rates of p16 were 83.08%, 81.97%, 78.13%, 89.09%, 69.23%, and 40.00%, respectively. All the expression of these 3 genes showed significant difference between GED stage II-III and GED stage I, GC and GED stage II-III. In the same pathological changes, the positive expression rate of these 3 genes was higher in Hp infection group than in no Hp infection group, while there was no significant difference (P > 0.05).

Conclusion: The mutation of p53 and inactivation of p21WAF1 and p16 play an important role in carcinogenesis of stomach. However, Hp infection was not associated with the abnormal expression of these 3 genes.

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