Helicobacter pylori and gastric malignancies.

The epidemiological link of Helicobacter pylori and gastric carcinoma was confirmed and the reported rate of gastric carcinoma development in the Japanese population with H. pylori gastritis was 2.9% during a 7.8-year period. Studies showed that gastric atrophy and intestinal metaplasia may partially regress after H. pylori eradication, but whether this will result in a decrease in the development of malignant lesions remains to be confirmed in large studies. Little progress was made towards the identification of criteria applicable to individualized populations that would benefit from H. pylori screening and surveillance of gastric malignancy. Studies of low-grade MALT lymphoma reported clinical and molecular features that may be useful to identify cases that may be responsive to H. pylori eradication therapy, namely evaluation of lymphoma stage by EUS and t(11;18). The role of H. pylori eradication therapy in high-grade MALT lymphoma needs to be evaluated in larger prospective studies. The application of methods of global analysis of gene expression (microarray studies) resulted in the explosion of information on the molecular pathways activated by H. pylori in gastric epithelial cells. New pathways that may play an important role in H. pylori carcinogenesis have been discovered in several studies.