ABSTRACT The bacterium Helicobacter pylori ( Hp ) infects half the world and causes stomach inflammation. Most infections are asymptomatic, but in 1%–2% of infected individuals, inflammation can lead to a cascade of tissue changes that culminates in the development of metaplasia (pre-cancer) and finally gastric cancer, a highly fatal disease. It has been posited that Hp ’s role in the process is merely to initiate inflammation, and once the later stages of disease develop, Hp becomes dispensable. However, epidemiological and molecular studies support a different paradigm: that in at least some individuals, Hp actively drives metaplasia and carcinogenesis. Molecular profiling shows that Hp is prevalent during gastric cancer. In individuals with metaplasia, successful antibiotic eradication of Hp prevents the development of gastric cancer; antibiotic eradication after cancer appears can even significantly reduce the likelihood of tumor recurrence. In rodent models of gastric cancer, Hp infection accelerates carcinogenesis, and in a metaplasia model, Hp infection alters the metaplastic lineages present and causes increased dysplasia (abnormal cells). Taken together, these data point to an active role for Hp infection in driving gastric cancer development, at least in some individuals. Therefore, studies investigating host-pathogen interactions in the context of Hp -driven carcinogenesis should encompass the entire spectrum of disease development, not just the establishment of gastric infection and initiation of inflammation. Understanding the complete picture of Hp -driven disease will enable us to tackle this highly fatal cancer.
Valerie P. O’Brien (Mon,) studied this question.