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Gut 2001;48:290-292; doi:10.1136/gut.48.3.290
Copyright © 2001 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2001;48:290-292 ( March )

Commentary

See article on page 297

Helicobacter pylori associated gastric B cell MALT lymphoma: predictive factors for regression

The first 150 words of the full text of this article appear below.

Experimental data have extended the knowledge of the mere association of gastric mucosa associated lymphoid tissue (MALT) lymphoma and infection with Helicobacter pylori. The acquisition of MALT in the stomach is a direct consequence of the infection; thus MALT in the stomach is formed as an immunological defence system to control local infection caused by H pylori. Lymphomas arising from gastric MALT show several specific features: they arise from the marginal zone of the lymphoid follicle, they consist of centrocyte-like cells, and lymphoepithelial destruction must be present in order to establish the diagnosis of gastric MALT lymphoma.1 2 The genetic events that lead to clonal evolution and, finally, malignant transformation also show that MALT lymphomas have specific features not known from nodal lymphomas---for example, the translocation t(11;18). Data concerning other genetic events like rearrangements of oncogenes such as bcl-2 (translocation t(14;18) in follicular lymphoma), c-my (translocation t(8;14) in Burkitt's lymphoma), . . . [Full text of this article]


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Predictive factors for regression of gastric MALT lymphoma after anti-Helicobacter pylori treatment
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