AIM:To study the relationship between Helicobacter pylori(H.pylori)and gaatric carcinoma and its possiblepathogenesis by H.pylori.METHODS:DNEL technique and immunohistochemicaltechnique were used to study the state of apoptosis,proliferation and p53 gone expression.A total of 100 gastricmucosal biopsy specimens,including 20 normal mucosa,30H.pylori-negative and 30 H.pylori-positive gastricprecancerous lesions along with 20 gastric carcinomas werestudied.RESULTS:There were several apoptotic cells in thesuperficial epithelium and a few proliferative cells within theneck of gestric glands,and no p53 protein expression innormal mucosa.In gestric carcinoma,there ware fewapoptotic cells,while there were a large number ofproliferative cells,and expression of p53 proteinsignificantly was increased.In the phase of metaplasia,theapoptotic index(Al,4.36%±1.95%),proliferative index(Pl,19.11%±6.79%)and positivity of p53 expression(46.7%)in H.pylori-positive group ware higher than thosein normal mucosa(P<0.01).Al in H.pylori-positive groupwas higher than that in H.pylori-negative group(3.81%±1.76%),Pl in H.pylori-positive group was higher than thatin H.pylori-negative group(12.23%±5.63%,P<0.01).Inthe phase of dysplasia,Al(2.31%±1.10%) in H.pylori-positive group was lower(3.05%±1.29%)than that in H.pylori-negative group,but Pl(33.89%±11.65%)wassignificantly higher(22.09±8018%,P<0.01).In phases ofmetaplasia,dysplasia and gastric cancer in the H.pylori-positive group,Als had an evidently greduall decreasingtrend(P<0.01),while Pls had an evidently gradualincreasing trend(P<0.05 or P<0.01),and there was alsoa trend of gradual increase in the expression of p53 gone.CONCLUSION:In the course of the formation of gastriccarcinoma,proliferation of gastric mucosa can be greatlyIncreased by H.pylori,and H.pylori can induce apoptosisin the phase of metaplasia,but in the phase of dysplesia H.pylorl can inhibit cellular apptosis.And H.pylori infectioncan strengthen the expression of mutated p53 gene. AIM: To study the relationship between Helicobacter pylori (H. pylori) and gaatric carcinoma and its possible pathogenesis by H. pylori. METHODS: DNEL technique and immunohistochemical techniques used to study the state of apoptosis, proliferation and p53 gone expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30 H. pylori-negative and 30 H. pylori-positive gastric precancerous lesions along with 20 gastric carcinomas were staged .RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of the gestric glands , and no p53 protein expression innormal mucosa. In gestric carcinoma, there are few numbers of proliferating cells, and there was a large number of proliferative cells, and expression of p53 proteins wereificantly increased. The phase of metaplasia, the apoptotic index (Al, 4.36% ± 1.95 %), proliferative index (Pl, 19.11% ± 6.79%) and positivity of p53 expression (46.7%) in H.pylori-positive group ware higher than thosein normal m (p <0.01) .Al in H.pylori-positive group was higher than that in H.pylori-negative group (3.81% ± 1.76%), Pl in H.pylori-positive group was higher than that in H.pylori-negative group (2.31% ± 1.10%) in H. pylori-positive group was lower (3.05% ± 1.29%) than that in H. pylori-negative (12.23% ± 5.63%, P < group, but Pl (33.89% ± 11.65%) wassignificantly higher (22.09 ± 8018%, P <0.01) .In phases of metaplasia, dysplasia and gastric cancer in the H.pylori-positive group, Als had an evidently greduall depresstrend (P < 0.01) while there was an evidently gradualincreasing trend (P <0.05 or P <0.01), and there was also a trend of gradual increase in the expression of p53 gone. CONCLUSION: In the course of the formation of gastriccarcinoma, proliferation of gastric mucosa can be greatly Increased by H. pylori, and H. pylori can induce apoptosis in the phase of metaplasia, but in the phase of dysplesia H. pylorl can inhibit cellular apptosis. And H. pylori infection scan strengthen the expression of muta ted p53gene.