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Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) commonly arises from a background of chronic inflammatory disorder at various mucosal sites. The cause of the chronic inflammatory disorder is highly site dependent, ranging from microbial infection to autoimmune response. The adaptive immune responses generated by these different chronic inflammatory processes most likely have a critical impact on the clonal evolution of the lymphoma cells and their acquired somatic genetic changes. There is growing evidence showing biased usage of immunoglobulin genes, thus expression of stereotypic autoreactive B-cell receptor (BCR), in MALT lymphoma of various sites. There are also mounting data demonstrating distinct somatic genetic profiles among MALT lymphoma of different sites. More recent studies have revealed an association between biased immunoglobulin gene usage and somatic genetic changes that promote BCR signalling in ocular adnexal MALT lymphoma. Furthermore, there are distinct genetic changes in MALT lymphoma of the salivary gland and thyroid, which involve immune receptors and may enable them to gain more help signals from their microenvironment. In this review, I will summarise the recent research advances, advocating for a critical role of oncogenic cooperation between immunological drive and genetic changes for clonal evolution of MALT lymphoma cells.

Mucosa-associated lymphoid tissue lymphoma of various sites: common molecular mechanisms but different players