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Pulmonary MALT Lymphoma : Pathogenesis

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Pulmonary MALT Lymphoma - Pathogenesis : Normal lung contains a rich network of lymphatic channels that propels lymphatic fluid centrally towards septal, hilar, and mediastinal lymph nodes. In addition, there are sparse submucosal lymphoid aggregates. However, there is no organized mucosa-associated (or bronchus-associated) lymphoid tissue (MALT or BALT) in normal lung. MALT may be acquired as a response to smoking, infections, or autoimmune disorders. It consists of B-cell-rich secondary lymphoid follicles with germinal centers, a well-defined marginal zone of activated and memory B cells, and T-cell-rich interfollicular areas.

Unlike Helicobacter pylori and gastric MALT lymphomas, no specific etiologic agent has been definitively linked to pulmonary MALT lymphomas, although one study found a higher prevalence of gram-negative bacterium Achromobacter xylosoxidans in the biopsies of pulmonary MALT lymphoma as compared to non-lymphoma biopsies.

The underlying pathogenetic mechanisms appear to be similar to H. pylori and gastric MALT lymphomas. Chronic antigenic stimulation leads to lymphoid hyperplasia and sets up conditions for the eventual emergence of a neoplastic B-cell clone. Several chromosomal translocations, e.g. t(11;18), which upregulate BCL10 and/or MALT1 expression that play a role in the pathogenesis of MALT lymphomas have been identified. Both proteins participate in NF-κB signaling pathway that promotes B-cell survival and growth.

The image shows neoplastic marginal zone cells colonizing lymphoid follicles in a case of pulmonary MALT lymphoma. Several residual germinal centers can be seen.

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