Abstract
Chronic gastric infection by the gram-negative bacterium Helicobacter pylori is strongly associated with the development of distal gastric carcinoma and gastric mucosal lymphoma in humans. Eradication of H. pylori with combination antibiotic therapy cures most cases of gastric lymphoma and slows progression to gastric adenocarcinoma. H. pylori promotes gastric neoplasia, principally via the induction of an intense gastric inflammatory response that lasts over decades. This persistent inflammatory state produces chronic oxidative stress and adaptive changes in gastric epithelial and immune cell pathobiology that in a minority of infected subjects eventually proceeds to frank neoplastic transformation.