| [ Summary ] |
Many of the sites where mucosa-associated lymphoid tissue (MALT) derived lymphoma occurs lack any native lymphoid tissue. Therefore, before lymphoma occurs, lymphoid tissue must be acquired. Several studies have shown that the incidence of MALT lymphoma is linked to a high prevalence of H. pylori infection. Epidemiological studies have shown that H. pylori infection increases the risk of developing any type of gastric lymphoma. Several animal experiments also have demonstrated that Helicobacter species including H. pylori developed MALT and MALT lymphoma. This evidence supports the theory that gastric lymphoma derives from acquired MALT. Growing worldwide evidence shows that the successful cure of H. pylori infection results in the regression of MALT lymphoma in 70 - 90 % of patients.
Although the mechanism by which H. pylori infection causes MALT lymphoma has not been completely elucidated, several studies suggest that MALT lymphoma B-cells directly respond to H. pylori but require the help of T-cells to make a proliferative response, or that H. pylori is antigenically stimulating nonneoplastic T-cells to release cytokines that stimulate the proliferation and transformation of B-cells. An understanding of this biological mechanism is very important for the management of gastric MALT lymphoma. |