Abstract
Helicobacter pylori (H. pylori) infects more than half of the world’s human population, but only 1 to 3% of infected persons develop gastric adenocarcinoma. H. pylori is a definite or class I carcinogen in humans. The mechanisms of H. pyloriassociated gastric carcinogenesis are still poorly defined. The clinical outcome of the infection is determined by host genetic predisposition (IL-1β, TNFα, IL-10), bacterial virulence factors (VacA, CagA), as well as environmental factors (salt intake, smoking). Eliminating H. pylori from a large part of the population may be unfeasible economically, and the long-term consequences are still unpredictable; this is why identifying high-risk individuals is very important.
Keywords: Adhesins, gastric cancer, Helicobacter pylori, helminths infection, interleukins, outer membrane proteins, peptidoglycans, polymorphisms, salt intake, smoking, tumor necrosis factor-ά, virulence factors.