Abstract
Abstract 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
