Oncogenic mechanisms of MYC in aggressive mature B-cell lymphomas. (A) In BL and DLBCL, MYC is activated by gene translocations or amplifications. Activation of the TCF3/ID3 pathway cooperates with MYC in BL, whereas BCL2 and/or BCL6 translocations are the cooperating mechanisms in DLBCL. (B) In PBL, MYC is activated by translocations, whereas in ALK-positive large B-cell lymphomas, MYC is up-regulated indirectly by the oncogenic effect of ALK and STAT3 activation. In both tumors, MYC activation overcomes the suppressor effect of BLIMP1. The activation of the unfolded protein response may be a survival mechanism to counterbalance the proapoptotic function of MYC. Stars represent somatic mutations and green and red boxes indicate activating and suppressing mechanisms, respectively.