Gastric MALT lymphoma, a clinical and morphological entity of B-cell lymphomas, is originated from the follicular marginal zone. There is a close relationship between Helicobacter pylori (H. pylori) infection and MALT lymphoma. The chronic presence and activity of the bacterium increases the risk of lymphomagenesis. More than 90% of MALT lymphoma patients are infected with H. pylori. It is highly probable that the pathomechanism of gastric MALT lymphoma has the following schedule: a) first step is the accumulation of MALT cells due to H. pylori infection (normal gastric mucosa has no MALT); b) the accumulation of B-cells (resembling marginal zone cells) is T-cell dependent; T-cells recognise the bacterial antigens. At this stage the eradication of H. pylori can result in the disappearance of the lymphoid (MALT) tissue (now called as MALT lymphoma), c) If the stimulation of B-cell proliferation continues, the possibility to acquire genetic errors is increasing, leading to a more-And-more T-independent stage, with autonomy, and the potential to be transformed to a high malignancy form. It is a question, whether at the first stage (when anti-H. pylori therapy can cure the MALT lymphoma) represents a "benign" lymphoma (prelymphoma) or an already malignant lymphoproliferation.
|Translated title of the contribution||Helicobacter pylori and gastric MALT lymphoma|
|Number of pages||6|
|Publication status||Published - Dec 1 1999|
ASJC Scopus subject areas