Gastric carcinogenesis involves a slow but continuous, stepwise evolution from superficial gastritis to glandular atrophy, metaplasia, dysplasia, and finally, to adenocarcinoma. In 1994, the International Agency for Research on Cancer defined Helicobacter pylori (H. pylori) as a group I carcinogen. Evidence supporting a causal association has been demonstrated by epidemiological data as well as by experimental animal models. The process of carcinogenesis, which may well extend over decades, provides an excellent opportunity for prevention or early detection of the events preceding development of the neoplasm. This is especially true because, at present, H. pylori can be readily treated. Despite this, the prognosis for gastric cancer is poor and, in most industrialised countries, the survival is only 10% after 5 years from diagnosis. The sole exception is Japan where this malignancy is often identified at an early stage when cure by radical surgery is more probable.