Recent epidemiologic evidence indicates that Helicobacter pylori infection increases the risk for gastric carcinoma. Infection with H. pylori leads to chronic gastritis, which usually persists for life unless treated with antimicrobial drugs. Because the great majority of gastritis patients never develop neoplasias, research concerning those who do may provide clues about carcinogenesis. In affluent populations, H. pylori infection leads to nonatrophic gastritis, predominantly involving diffusely the antrum (diffuse antral gastritis), the basic lesion seen in patients with duodenal ulcer, which has not been associated with increased risk for gastric carcinomas. In populations with high gastric cancer risk, H. pylori infection is associated with multifocal atrophic gastritis, which frequently advances to intestinal metaplasia, occasionally to dysplasia, and rarely to carcinoma. H. pylori infection increases the rate of proliferation of the gastric epithelial cells and decreases the gastric secretion of ascorbic acid, processes that may modulate the process of carcinogenesis. Infection with H. pylori is characterized by infiltration of lymphocytes, polymorphonuclear leukocytes, and macrophages in the gastric mucosa. There is considerable interest in investigating oxygen radicals originating in white blood cells and the possibility that they induce mutations with carcinogenic potential in the gastric epithelium.