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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-alpha. 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.
Peek et al. (Sat,) studied this question.