Figure 4.

Aberrant BCR signaling in GC‐derived B‐cell lymphomas. BCR signaling is essential for mature B‐cell survival. Most GC‐derived lymphomas hijack BCR and/or PI3K signaling, including: BL, FL, the ABC‐DLBCL subtypes C5 and MCD, and the GCB‐DLBCL subtypes C3 and EZB. Depicted are the most frequent mutations that promote aberrant BCR/PI3K signaling activation in these lymphomas. Alterations that affect indirect modulators of the PI3K pathway such as PTEN and MIR17HG are more reminiscent of antigen‐independent “tonic” BCR signaling than antigen‐dependent “chronic‐active” BCR signaling. *MYD88 is mutated in ABC‐DLBCL but not in FL. Concurrent mutations of CD79A/B and MYD88 are most common in C5 and MCD lymphomas and less so in other lymphomas. BL, Burkitt lymphoma; FL, follicular lymphoma; DLBCL, diffuse large B‐cell lymphoma