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

Abstract

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.
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.
(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).
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.