The carcinogenic effect of H. pylori on the gastric epithelial cell.
The recent demonstration in animal models that H. pylori alone may be capable of inducing intestinal-type gastric cancer, and that H. felis can accelerate gastrin-induced gastric neoplasia has stimulated research on examining the mechanisms of H. pylori-associated carcinogenesis in humans. Several mechanisms are currently under investigation, including the dysregulation of the gastric epithelial cell cycle, the formation of DNA adducts, the generation of free radicals, alterations in growth factor secretion and cytokines, and the effects of decreased gastric acid secretion. This review will examine the relevant evidence acquired from human tissue studies, animal models and cell culture systems in an attempt to explore these pathways, and to evaluate the mechanisms by which H. pylori may cause gastric cancer.
Moss
S F
SF
Department of Medicine, St. Luke's-Roosevelt Hospital Center/ Columbia University, New York, NY 10025, USA. smoss1@pol.net
D000818:Animals; D002455:Cell Division; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D013274:Stomach Neoplasms / Q000382:microbiology*