These data suggest that Igβ and CD19 are part of an alternative B-cell signaling module that use continuous ITAM/PI3K signaling to promote the survival of B lymphoma and normal B cells.
A meta-analysis of the literature shows a significantly high frequency of concurrent MYD88L265P and CD79B ITAM mutations in primary CNS lymphoma and testicular DLBCL, underscoring the role of B cell receptor and nuclear factor kB activation by somatic mutations in these lymphomas that colonize immune-privileged sites.
These results reveal that CD79B and surface IgM constitute a rate-limiting checkpoint against B cell dysregulation by <i>MYD88<sup>L265P</sup></i> and provide an explanation for the co-occurrence of <i>MYD88</i> and <i>CD79B</i> mutations in lymphomas.
Mutations in 2 upstream components of the nuclear factor κB (NF-κB) pathway, CD79B and MYD88, are important information for new target therapy in malignant lymphoma.