engleski

The API2-MALT1 fusion protein as inducer of an independant mechanism in pathogenesis of gastric MALT type lymphoma – case report

A 46 year old male patient was observed during 29 months due to H. pylori infection and MALT lymphoma. During this period he become H. pylori negative, clinical and endoscope findings regressed almost normal, however morphological features of MALT type lymphoma persist. Molecular analysis of IgH CDR3 region did not confirm clonal rearrangement. All samples were Bcl10 negative, while FISH detected translocation t(11 ; 18)(q21 ; q21) but not the translocation t(14 ; 18)(q32 ; q21). Pathogenesis of GI MALT type lymphoma is connected to three specific translocations: t(11 ; 18)(q21 ; q21) results in a chimeric API2-MALT1 gene fusion, t(1 ; 14)(p22 ; q32) juxtaposes Bcl10 to an IgH gene locus and t(14 ; 18)(q32 ; q21) includes MALT1 and IgH gene. These translocations are, on molecular level, the part of NFκ B activation through physiological role of Bcl10 and MALT1 genes. The Bcl10/MALT1 complex represents the most frequent mechanism for NFκ B activation and is considered responsible for development of MALT type lymphoma. Alternative mechanism is believed to be Bcl10 independent and induced by API2-MALT1 fusion protein. Although t(11 ; 18)(q21 ; q21) is often accompanied by nuclear Bcl10 expression, the results of our case indicate the alternative pathway of NFκ B activation.

API2-MALT1 fusion protein; MALT lymphoma

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