The mucosa-associated lymphoid tissue (MALT) lymphomas are thought to arise from the extranodal counterpart to post-follicular memory B cells found in the marginal zone of lymph node follicles. These tumors are often localized and their behavior is generally indolent. At least some depend on continued antigen stimulation for survival, as demonstrated by the prolonged complete responses that are seen when early-stage gastric MALT lymphoma is treated with an antibiotic regimen to eradicate chronic Helicobacter pylori infection.
t(11;18)(q21;q21) is found in more than half of all low-grade MALT lymphomas, with a preference for gastric lymphomas. The translocation is not typically found in high-grade MALT lymphomas. API-2-MALT 1 fusion protein is expressed from the mutant locus. API-2 (also known as IAP-2) belongs to a family of inhibitors of apoptosis that prevent death, likely due to their direct interaction with caspases, the proteases activated by programmed cell death. The physiological function of the MALT 1 protein is less well understood, though it possesses a caspase-like domain at its C-terminus. The function of the fusion protein is unclear, though there is some evidence that it activates NF-kB, perhaps leading to inhibition of ap-optosis.
BCL-10 is overexpressed in a minority of MALT lymphoma cases via the t(1;14)(p22;q32), putting the coding region of BCL-10 under the influence of the immunoglobulin heavy chain enhancer. The function of this protein is unclear, but some have suggested an interaction between BCL-10 and MALT-1, leading to NF-kB activation. Others have shown that API2-MALT 1 correlates with the nuclear location of BCL-10. These findings suggest that these two translocations may be involved in activating the same pathway.
Trisomy 3 is observed in 20-60% of all MALT lymphomas. The oncogenic properties of this numerical chromosomal abnormality are not understood.
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