Helicobacter pylori infection and gastric carcinoma

Abstract

Helicobacter pylori infection is considered to be the main cause of gastric cancer and the most frequent infection-induced cancer. H. pylori is a heterogeneous species which can harbour pathogenic factors such as a cytotoxin, a pathogenicity island (cag) encoding a type 4 secretion system, and the first bacterial oncoprotein, CagA. This oncoprotein appears to be involved in the carcinogenic process in addition to the inflammation generated. This process may concern either local progenitors via an epithelial-mesenchymal transition, or recruited bone marrow-derived mesenchymal cells. There are also environmental factors such as iron deficiency or high-salt diets which interact with the bacterial factors to increase the risk of gastric cancer as well as genetic polymorphism of certain cytokines, e.g. IL-Iβ. Recent data suggest that a break in coevolution of a particular phylogeographic lineage of H. pylori and its usual host may also be a risk factor. Studies are currently being performed to assess the feasibility of organized H. pylori eradication programmes to prevent gastric cancer.

Keywords: CagA oncoprotein; VacA cytotoxin; cancer stem cells; carcinogenesis; epithelial–mesenchymal transition; prevention.