Helicobacter pylori and Gastric Carcinoma

A large amount of epidemiological evidence has accumulated indicating a significant relationship between Helicobacter pylori (Hp) infection and chronic gastritis [1,2], peptic ulcers [3], intestinal metaplasia [4,5], and adenocarcinoma [6–8] or lymphoma [9] development. In 1994, the World Health Organization/International Agency for Research on Cancer concluded that “Hp is a definite carcinogen” based on the epidemiological findings [10]. Hp infection almost always results in chronic antral gastritis, but only a proportion of patients develop stomach cancer, so it is clear that the bacterium cannot be the only causative factor. To demonstrate a “causal link” between Hp infection and stomach carcinogenesis, as well as intervention studies, it is essential to establish an experimental animal model. In Mongolian gerbils (MGs), Hp infection, chronic active gastritis, peptic ulcers, and intestinal metaplasia closely mimic those in man [11]. In this chapter, epidemiological and experimental evidence associated with Hp infection and gastric carcinogenesis is reviewed.