MALT LYMPHOMA: MANY ROADS LEAD TO NF-kB ACTIVATION
Résumé
Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) is genetically characterised by several recurrent, but mutually exclusive chromosome translocations. To date, it has been shown that at least the oncogenic products of t(1;14)(p22;q32)/BCL10-IGH, t(14;18)(q32;21)/IGH-MALT1 and t(11;18)(q21;q21)/API2-MALT1 activate the NF-kB activation pathway. Recently, A20, an essential global NF-kB inhibitor, was found to be inactivated by somatic deletion and/or mutation in translocation negative MALT lymphomas. However, these genetic abnormalities alone are not sufficient for malignant transformation and thus need to cooperate with other factors in MALT lymphomagenesis. Recent studies have shown steady exciting progresses in our understanding of the biological functions of BCL10, MALT1 and A20 in the regulation of the NF-kB activation pathways and the biology of lymphocytes. This review discusses the implication of these recent advances in the molecular pathogenesis of MALT lymphoma, and explores how the above genetic abnormalities cooperate with immunological stimulation in the lymphoma development.
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