Gastric lymphoma and Helicobacter pylori.

The clinical and experimental work suggests the following scheme for the pathogenesis of gastric lymphoma. The first step is accumulation of lymphoid tissue (MALT) in response to infection of the stomach by H. pylori. In rare instances, this lymphoid infiltrate contains cells with a growth advantage, possibly because of a genetic change (trisomy 3?). The result is a monoclonal lymphoproliferative lesion that is responsive to H. pylori-driven T-cell help. Further genetic changes [t(1;14)?] may lead to escape from T-cell dependency and, ultimately, high-grade transformation. Low-grade B-cell gastric lymphoma serves as the paradigm for the entire group of MALT lymphomas that occur in a wide variety of extranodal sites. It is likely that the growth of this group of lymphomas is governed by a series of different antigens, many of which, like H. pylori, might be microbiologic. The challenge is to identify these agents and apply this knowledge to the treatment of other MALT lymphomas. This work also emphasizes the importance of paying attention to the histologic structure and nature of the ancillary cells in low-grade B-cell lymphomas. These cells, particularly the T cells, are not accidental passengers or necessarily representative of a "host response" to the neoplastic B cells. In low-grade MALT lymphomas, they are vital for the survival of the tumor. Similar mechanisms may be operative in nodal low-grade B-cell lymphomas and could offer new approaches to therapy.