Figure 3.
Molecular background of DPE in DLBCL. (A) Oncoprint of the most common driver gene alterations in the discovery cohort stratified according to DPE status. Drivers with mutations observed in ≥10% of the cases included. Patients with complete genomic data and BCL2 and MYC immunohistochemical data included. (B) Genetic drivers differentially mutated (Fisher’s exact, P < .1) between DA and non-DA GCB BCLs. Driver mutations observed in ≥3% of the cases in the GCB subtype according to the Hans algorithm with complete cytogenetic and immunohistochemical data of BCL2 and MYC included for the analysis. (C) Hierarchical clustering of the gene set exemplars according to double protein expression status. The exemplars and their expressions were recognized with affinity propagation clustering in Reddy et al. (D) Box plot demonstrating the difference in expression of “MYC/nucleotide biosynthesis” gene set between DPE and non-DPE DLBCLs. (E) Box plot demonstrating the difference in expression of host response-related gene set between DPE and non-DPE DLBCLs. (F) Box plot demonstrating the difference in expression of host response-related gene set between ABC and GCB DLBCLs among DPE DLBCL. Red dots indicate concurrent structural variants of BCL2 and MYC (DA BCLs). **P < .01; ***P < .001; ****P < .0001.