Helicobacter pylori and gastric malignancies.

Despite decreasing incidence during the last 50 years, gastric cancer still ranks as one of the most frequent cancers. A multifactorial model of human gastric carcinogenesis is currently accepted in which different dietary and nondietary factors, including genetic susceptibility of the host and Helicobacter pylori infection are involved at different stages in the cancer process. On the molecular level, at least two phenotypes, associated with distinct pathways of genome destabilization, have been identified. However, applying new technologies such as cDNA microarrays a new era in the analysis of molecular markers has started. This molecular technology may open the path towards novel treatment modalities, i.e. gene therapy. Epidemiological, biological, and molecular genetic studies have also implicated the role of H. pylori in lymphomagenesis. Knowledge of pathogenesis and therapy is increasing while good epidemiological data are rare. Many studies have demonstrated that MALT-type lymphomas develop along two different pathways: t(11;18)-positive cases, and t(11;18)-negative cases. Meanwhile, a third translocation could be detected, the t(14;18), opening the discussion of a possible third pathway of lymphoma development.