• gastric cancer

Helicobater pylori infection leads in some individuals to the development of gastric cancer.¹ Because both H pylori infection and gastric cancer are relatively common worldwide, this association has spurred considerable interest into determining whether gastric cancer can be prevented by the eradication of H pylori and into investigating the mechanisms by which this extracellular bacterium and its associated inflammatory response promote carcinogenesis. In this regard, H pylori may provide important clues for the pathogenesis of other tumours associated with chronic inflammatory states.

Despite the fact that H pylori does not invade epithelial cells, it has important and profound effects on the gastric epithelial cell, which include provoking a state of chronic epithelial hyperproliferation that has long been recognised as a precursor of malignancy in the stomach as it has in many other cancer prone organs. How does H pylori induce proliferation? A considerable amount of evidence from cell culture and animal models implicates apoptosis as the primary response of gastric epithelial cells to H pylori, with epithelial hyperproliferation as a secondary, presumably compensatory, occurrence.² The attachment of H pylori is generally thought to be necessary for the induction of apoptosis in gastric cells, based on experiments in co-culture systems. However, the downstream pathways involved in the transduction …