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Helicobacter infection and gastric neoplasia
Author(s) -
Peek Richard M,
Crabtree Jean E
Publication year - 2006
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1868
Subject(s) - helicobacter pylori , cancer , gastritis , chronic gastritis , immune system , inflammation , adenocarcinoma , pathogenesis , carcinogenesis , immunology , stomach , biology , genotype , medicine , gastroenterology , gene , genetics
Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for adenocarcinoma of the distal stomach, yet only a minority of people who harbour this organism ever develop cancer. H. pylori isolates possess substantial genotypic diversity, which engenders differential host inflammatory responses that influence clinical outcome. H. pylori strains that possess the cag pathogenicity island and secrete a functional cytotoxin induce more severe gastric injury and further augment the risk for developing distal gastric cancer. However, carcinogenesis is also influenced by host genetic diversity, particularly involving immune response genes such as IL‐1ß and TNF‐ α. It is important to gain insight into the pathogenesis of H. pylori ‐induced gastritis and adenocarcinoma, not only to develop more effective treatments for gastric cancer, but also because it might serve as a paradigm for the role of chronic inflammation in the genesis of other malignancies that arise within the gastrointestinal tract. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.