Activating mutations in CD79 and MYD88 have recently been found in a subset of diffuse large B-cell lymphoma (DLBCL), identifying B-cell receptor and MYD88 signalling as potential therapeutic targets for personalized treatment. Here, we report the prevalence of CD79B and MYD88 mutations and their relation to established clinical, phenotypic and molecular parameters in a large panel of DLBCLs. We show that these mutations often coexist and demonstrate that their presence is almost mutually exclusive with translocations of BCL2, BCL6 and cMYC, or Epstein–Bar virus infection. Intriguingly, MYD88 mutations were by far most prevalent in immune-privileged site-associated DLBCL (IP-DLBCL), presenting in central nervous system (75%) or testis (71%) and relatively uncommon in nodal (17%) and gastrointestinal tract lymphomas (11%). Our results suggest that MYD88 and CD79B mutations are important drivers of IP-DLBCLs and endow lymphoma-initiating cells with tissue-specific homing properties or a growth advantage in these barrier-protected tissues.

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A significant correlation was observed between interstitial infiltrates of CD20+ cells and CD3+ cells (r=0.720, P<0.001) suggesting that if B-cell infiltrates are present during rejection, they occur with T-cell infiltrates in a concurrent fashion. In contrast to previous reports, no relation was found between the number of CD20+ cells, in aggregates or in a scattered interstitial pattern, and response to conventional therapy. Remarkably, CD3+T cell aggregates did predict a favorable renal outcome.

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