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Helicobacter pylori-related gastric cancer results from a chronic inflammatory process that arises from atrophic gastritis, and develops into intestinal metaplasia, hyperplasia, and eventually gastric adenocarcinoma. Although approximately half of the world’s population is infected with Helicobacter pylori(H. pylori), less than 3% of these infected individuals develop gastric cancer. H. pylori infection can cause both acute and chronic inflammation, and may be present for decades within its host. Inflammatory gene variants are particularly important factors that may influence a host’s susceptibility to H. pylori-related gastric cancer. The inflammatory gene variants uncovered thus far include interleukin gene clusters, tumor necrosis factor-α, Toll-like receptors(TLRs), and inflammatory gene polymorphisms found in genome-wide association studies(GWAS). The association between these gene variants and the risk of H. pylori-related gastric cancer will aid in our understanding of the pathogenesis of gastric cancer in order to prevent and defeat this malignancy.
Helicobacter pylori-related gastric cancer results from a chronic inflammatory process that arises from atrophic gastritis, and develops into intestinal metaplasia, hyperplasia, and eventually gastric adenocarcinoma. Although approximately half of the world’s population is infected with Helicobacter pylori (H. pylori), less than 3% of these infected individuals develop gastric cancer. H. pylori infection can cause both acute and chronic inflammation, and may be present for 10 within its host. Inflammatory gene variants are more important factors that may influence a host’s susceptibility to H. pylori -related gastric cancer. The inflammatory gene variants uncovered thus far include interleukin gene clusters, tumor necrosis factor-α, Toll-like receptors (TLRs), and inflammatory gene polymorphisms found in genome-wide association studies (GWAS). The association between these gene variants and the risk of H. pylori-related gastric cancer will aid in our understanding of the path ogenesis of gastric cancer in order to prevent and defeat this malignancy.