Gastric low‐grade mucosa‐associated lymphoid tissue lymphomas: Their histogenesis and high‐grade transformation

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Abstract
Gastric low‐grade mucosa‐associated lymphoid tissue (MALT) lymphoma is a unique disease. A vast majority of lymphoma cells are centrocyte‐like cells or resemble monocytold B cells, and occasionally show plasmacytic differentiation. Immunophenotypical and immunogeno‐typical examinations have indicated that they are in the differentiation stage of memory B cells, whose normal counterparts are marginal zone lymphocytes or monocytoid B cells In the lymphoid tissues. It arises from chronic gastritis closely associated with Helicobacter pylori (H. pylori) infection. Mucosa‐associated lymphoid tissue lymphomas of other organs are also based on acquired MALT associated with chronic inflammation or autoimmune diseases. Interestingly, the majority of gastric low‐grade MALT lymphomas regress by the eradication of H. pylori. The lymphoma cells, however, are not derived from B cells reacting with H. pylori itself but from autoreactive B cells. Although the mechanism of their oncogenesis has not been clarified, previous data suggest that autoreactive B cells proliferate in response to H. pylori‐specific T cells, presumably with some cytoklnes. The genetic Instability of such B cells then induces chromosomal abnormalities including trisomy 3 and/or other genetic changes. These B cells have the ability of autonomic proliferation and, even so, they might be sensitive to T cell stimuli. Low‐grade gastric lymphomas occasionally progress to high‐grade malignancy. The high‐grade component of MALT lymphomas are composed of large‐sized lymphoma cells that are morphologically indistinguishable from nodal large B cell lymphomas. This high‐grade transformation is associated with p53 abnormalities or Bcl‐6 overexpresslon. Gastric MALT lymphoma may provide a useful model in understanding multistep lymphomagenesls.