Table 2

MYC activation and cooperating mechanisms in aggressive B-cell lymphomas

LymphomaNormal cell counterpartMYC inhibitory physiological mechanismMYC oncogenic activationMYC cooperating mechanism*
BL DZ GC cell BCL6 MYC translocation TCF3/ID3/CCND3 mutations 
GCB-DLBCL LZ GC cell BCL6 MYC translocation/? BCL2 translocation 
ABC-DLBCL LZ GC cell BCL6 BCR/MYD88 activation BCL2 overexpression (18q amplifications) 
PBL Plasmablast BLIMP1 MYC translocation ER stress response? 
ALK-positive large B-cell lymphoma Plasmablast BLIMP1 ALK-STAT3 activation? ER stress response? 
LymphomaNormal cell counterpartMYC inhibitory physiological mechanismMYC oncogenic activationMYC cooperating mechanism*
BL DZ GC cell BCL6 MYC translocation TCF3/ID3/CCND3 mutations 
GCB-DLBCL LZ GC cell BCL6 MYC translocation/? BCL2 translocation 
ABC-DLBCL LZ GC cell BCL6 BCR/MYD88 activation BCL2 overexpression (18q amplifications) 
PBL Plasmablast BLIMP1 MYC translocation ER stress response? 
ALK-positive large B-cell lymphoma Plasmablast BLIMP1 ALK-STAT3 activation? ER stress response? 

DZ indicates dark zone; and LZ, light zone.

*

TP53 and MYC mutations present in all types of lymphomas may help the tumor cells to escape the apoptotic effect of MYC.20,38 

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