Table 1.

MYC and BCL2 deregulation in DLBCL and HGBL

Morphology and immunophenotypeDLBCL (%)HGBL (%)
GCBABC
MYC protein by IHC 27 35 60 
 Mechanisms Translocation BCR and NF-κB signaling Translocation 
 Incidence of translocation 21 60 
BCL2 protein by IHC 43 63 70 
 Mechanisms
  
Translocation BCR and NF-κB signaling; gene amplification Translocation 
 Incidence of translocation 25 40 
DE-DLBCL 15 23 NA 
MYC and BCL2 translocations
  
6 (if de novo DLBCL) 21 (if prior FL*<1 30 
MYC and BCL6 translocations 2  
Morphology and immunophenotypeDLBCL (%)HGBL (%)
GCBABC
MYC protein by IHC 27 35 60 
 Mechanisms Translocation BCR and NF-κB signaling Translocation 
 Incidence of translocation 21 60 
BCL2 protein by IHC 43 63 70 
 Mechanisms
  
Translocation BCR and NF-κB signaling; gene amplification Translocation 
 Incidence of translocation 25 40 
DE-DLBCL 15 23 NA 
MYC and BCL2 translocations
  
6 (if de novo DLBCL) 21 (if prior FL*<1 30 
MYC and BCL6 translocations 2  

This table presents the incidence of MYC and BCL2 protein expression and their main mechanisms of deregulation by lymphoma subtype. Values are based on 1106 patients who had available data for MYC and BCL2 expression according to cell of origin subtype in 2 independent studies.8,10  In these studies, 529 of 1106 patients had the ABC subtype and 578 of 1106 had the GCB subtype. Of the GCB patients, 15% had DE-DLBCL, 6% would be reclassified as HGBL-DH with MYC and BCL2 translocations, and 2% would be reclassified with MYC and BCL6 translocations.

FL, follicular lymphoma; IHC, immunohistochemistry NA, not applicable.

*

In total, 21% of patients with DLBCL who have undergone histologic transformation from a previous follicular lymphoma (FL) are estimated to be HGBL-DH from the study by Pedersen et al.77 

Most of the GCB DLBCL with MYC and BCL6 translocations are triple hits and would be included in the 6% of patients with HGBL-DL harboring MYC and BCL2 translocations.

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