Helicobacter pylori causes gastric cancer by hijacking cell growth signaling

Extract: Infection with certain strains (carrying the cagA gene) of the bacterium Helicobacter pylori (H. pylori) is associated with the development of gastric carcinoma. Upon introduction into the gastric epithelial cells and its subsequent modification by phosphorylation (adding a phosphate group) at the tyrosine amino acid residue, CagA binds specifically to a cellular oncoprotein (SHP-2) and causes the oncoprotein's phosphatase activity (ridding is a phosphate group from a molecule) to misbehave. Interestingly, species of cagA-positive H. pylori isolated in East Asian countries exhibit stronger oncoprotein binding activity and greater pathological activity than those isolated in Western countries. H. pylori, a spiral-shaped bacterium that colonizes the human gastric mucosa, is estimated to inhabit at least half of the world's human population. H. pylori is primarily acquired in childhood and infection is lifelong in the majority of cases. In many cases, H. pylori is transmitted from infected parents to children. H. pylori infection can also be acquired via common environmental sources such as drinking water and animals particularly in developing countries. H. pylori infection causes gastric diseases such as chronic atrophic gastritis and peptic ulcers.