Primary Gastric Lymphoma.

The pathogenesis of gastric MALT lymphoma starts with accumulation of MALT following infection of the stomach by H. pylori. Rarely this lymphoid infiltrate contains cells with a growth advantage possibly due to a genetic change (trisomy 3?). The result is a monoclonal lymphoproliferative lesion which is responsive to H. pylori driven T-cell help. Because its growth is dependent on the presence of local antigen, gastric MALT lymphoma remains localized for long periods and it is during this phase that the lymphoma can be treated by eradication of H. pylori. Further genetic changes, as yet uncharacterized may lead to escape from T-cell dependency and ultimately high grade transformation.