Association Between Helicobacter Pylori Infection and Gastric Cancer

Helicobacter pylori infection is associated with a wide range of gastrointestinal diseasesincluding gastritis and peptic ulcer. H. pylori infection is also associated with development ofgastric cancer, especially in the younger generation, early gastric cancer, and noncardiacgastric cancer. There are two pathways by which H. pylori infection develops into gastriccancer: the indirect action of H. pylori on gastric epithelial cells causing inflammation, and thedirect action of the bacteria on epithelial cells. The H. pylori infection induces gastritis that itcan play crucial role in the development of gastric cancer. H. pylori infection contributes toparietal cell loss and hypochlorhydria. This leads to increased expression of growth factors,heparin-binding epidermal growth factor and transforming growth factor α; which is resultedto gastric metaplasia, dysplasia, carcinoma in situ, and gastric cancer. On the other hand, H.pylori can directly modulate epithelial cell function by bacterial agents such as CagA.Infection with cagA-positive H. pylori is associated with gastric adenocarcinoma and gastricmucosa-associated lymphoid tissue lymphoma of B cell origin. The cagA-encoded CagAprotein activates SHP-2 tyrosine phosphatase, an oncoprotein in human malignancies. CagAalso elicits junctional and polarity defects in epithelial cells. These CagA activities contributeto neoplastic transformation. Thus, CagA is a bacterium-derived oncoprotein which hasimportant role in development of H. pylori-associated neoplasms. H. pylori can provide asuitable environment, including chronic gastritis and neoplastic change. H. pylori infectionchanges many factors that are important to the pathogenesis of gastric cancer, includingvitamin C content of gastric juice and epithelial cell proliferation.

کلیدواژه ها:

Helicobacter Pylori ، Gastric Cancer ، CagA Protein ، Gastritis ، Neoplasia