[The relation between Helicobacter pylori infection and p53 mutation, MG-7 antigen and AgNORs expression in the development of gastric mucosa lesions].

OBJECTIVE: To explore the relation between H. pylori infection and the development of gastric mucosa lesions, and to evaluate the effect of H. pylori infection on cell proliferation, p53 mutation, and MG-7 antigen expression in patients with gastric precancerous lesions. METHODS: One hundred and nine gastric biopsy specimens were divided into five groups of different gastric mucosa lesions according to pathologic findings and the results of mucosa histochemical staining: type I intestinal metaplasia (IM), type IIIM, type III IM, dysplasia (Dys) and gastric cancer (GC). H. pylori and its cagA status were assessed by microdissection/PCR method. Expression of P53 protein and MG-7 antigen were examined by immunohistochemical staining. AgNOR staining was performed for each specimen. RESULTS: (1) Expression of P53 increased in more severe gastric mucosa lesion groups. The P53 expression rate in GC group was significantly higher than other groups (P < 0.05). There was no difference in expression of P53 between groups of different H. pylori status as while as different cagA status. (2) The expression of MG-7 in GC group was significantly higher than that in other groups (P < 0.05). There were no difference of expression of MG-7 between subgroups of different H. pylori infection status or cagA status in all groups (P > 0.05). (3) The counts of argyrophil protein of the nucleolar organizer regions (AgNORs) were significantly increased in more severe gastric mucosa lesion groups (P < 0.05), and were significantly higher in H. pylori positive and cagA positive specimens than in other specimens (P < 0.05). CONCLUSIONS: Infection with H. pylori, particularly cagA-positive strains, is associated with the development of more severe gastric mucosa lesions; it seems to have effects on cell proliferation in patients with gastric precancerous lesions. Expression of P53 and MG-7 are earlier events in gastric cancer carcinogenesis.