Infection with H. pylori plays a key pathogenic role and the infection has been classified by the International Agency for Research on Cancer (IARC) as a definite human carcinogen. It is associated with chronic atrophic gastritis, gastric mucosal atrophy and gastric cancer . It has been estimated that H. pylori infection may contribute to the occurrence of gastric cancer in 70% of cases. Although the majority of H. pylori-infected individuals have normal or increased acid secretion, a few become hypo- or achlorhydric and these people are thought to be at greatest risk. H. pylori-induced chronic inflammation with generation of reactive oxygen species and depletion of the normally abundant antioxidant ascorbic acid are also impoant. There is strong evidence that H. pylori eradication, especially if achieved before irreversible pre-neoplastic changes (atrophy and intestinal metaplasia) have developed, reduces the risk of cancer development in high-risk populations and is cost-effective. Diets rich in salted, smoked or pickled foods and the consumption of nitrites and nitrates may increase cancer risk. Carcinogenic N-nitroso-compounds are formed from nitrates by the action of nitrite-reducing bacteria that colonise the achlorhydric stomach. Diets lacking in fresh fruit and vegetables, as well as vitamins C and A, may also contribute. . No predominant genetic abnormality has been identified, although cancer risk is increased two- to threefold in first-degree relatives of patients, and links with blood group A have been repoed. Some host genetic factors related to inflammatory genes and prostate stem cell antigen have recently been associated with increased risk of gastric caner. Rarely, gastric cancer may be inherited in an autosomal dominant manner in association with mutations of the E-cadherin (CDH1) gene. H pylori infection also causes peptic ulcer,maltoma, gastric lymphomas Ref Davidson edition23rd pg782