Supplementary Tables S1-S2 and Supplementary Figures S1-S7 from EZH2 Inhibition by Tazemetostat Results in Altered Dependency on B-cell Activation Signaling in DLBCL

Table S1: Conditions and seeding densities of all cell lines used in studies; Table S2. Single agent IC50 values for agents tested for 3 days in 96-well plates as described in Materials and Methods; Figure S1. Tazemetostat dosing reduced H3K27me3 in tumor xenografts and is tolerated by SCID mice; Figure S2: CD40L has little effect on growth of DLBCL cell lines; Figure S3. SU-DHL-5 cells were treated for 4 days with TAZ (0.1 to 1 µM) followed by addition of 500 ng/mL CD40L at the indicated time points (1-60 minutes; Figure S4. An ABC-DLBCL gene signature (1) is up-regulated following tazemetostat treatment in KARPAS-422 (EZH2 mutant GCB), Farage (EZH2 WT GCB), SU-DHL-5 (EZH2 WT GCB), TMD8 (EZH2 WT ABC) and ABC vs. GCB gene signature was applied to RNAseq data from each cell line with and without tazemetostat treatment.; Figure S5: CD40L, but not IL-21 induces PRDM1 in combination with tazemetostat (TAZ); Figure S6. A CD40 responsive gene set (2) is up-regulated following tazemetostat treatment in KARPAS-422 (EZH2 mutant GCB), Farage (EZH2 WT GCB), SU-DHL-5 (EZH2 WT GCB), TMD8 (EZH2 WT ABC) and Basso_CD40¬_SIGNALING_UP gene signature was applied to RNAseq data from each cell line with and without tazemetostat treatment; Figure S7. Model for tazametostat mechanism of action in DLBCL