Molecular pathogenesis of mucosal-associated lymphoid tissue (MALT) lymphoma

Extranodal marginal zone B-cell lymphomas of mucosal-associated lymphoid tissue (MALT)-type occur in a number of anatomic sites, but share overlapping morphological and immunophenotypic features. Helicobacter pylori infection has been identified as an etiological factor in gastric MALT lymphoma, but the cause of MALT lymphomas at other sites remains a matter of speculation. Despite these limitations in understanding the etiology of MALT lymphoma, standard cytogenetic analysis has proved useful by demonstrating similar alterations in MALT lymphomas from different anatomic sites. The common cytogenetic alterations that characterize MALT lymphomas include t(11:18)(q21:q21), t(1;14)(p22;q32) and, more recently, t(14;18)(q32;q21). The apparent complexity of the cytogenetic alterations that have now been implicated in the pathogenesis of extranodal MALT lymphoma serves as a paradigm for molecular cross talk in neoplastic disease. Recent data have shown that these very disparate translocations affect a common signaling mechanism, and thus unify all three under a common pathogenesis, resulting in the constitutive activation of the NF-kappaB pathway.