Fig. 5: A7 DLBCL tumors are characterized by high c-myc expression and activity.

A Results of GSEA Hallmark pathway analysis presented as positive or negative association with A7 cluster membership. B c-myc gene expression by A7 status across clinical cohorts. In each cohort, MYC is expressesd at significantly higher levels in A7 compared to non-A7 (two-sided, unadjusted Wilcoxon p-values: ROBUST, <2.2e16; MER, 2.9e-7; REMoDL-B, 2.2e-9; GOYA, 5.5e-8; Reddy, 1.8e−9). C Representative c-myc IHC staining in multiple A7 cases and non-A7 cases; samples were selected for similar tumor cellularity. D Gene expression of TCF4 in patients plotted with copy number alteration status of TCF4 (ROBUST, N = 299), value in parentheses, copy number of TCF4;. Box plots represent the median and upper/lower quartiles, with whiskers extending to the most extreme values. **** indicates p  <  0.0001 (TCF4 Diploid vs. Gain, p = 1.8e−5; Diploid vs. Amplification, p = 4.4e−14), N.S., not significant (two-sided, unadjusted Wilcoxon test). E TCF4 mRNA expression in DLBCL cell lines, value in parentheses is the copy number of TCF4 in each model. F Western blot analyzing expression of TCF4 in ABC-DLBCL cell lines. Representative blots from 3 independent experiments. G, H Western blot analysis and quantitation of expression of MYC and TCF4 in TCF4 knockdown ABC-DLBCL cell lines. GAPDH, loading control. Represetative blots from 2 independent experiments. I Cell proliferation assay of control (shNT) and TCF4 knockdown (shTCF4) in ABC-DLBCL cell lines. Each point represents the mean of technical triplicates with standard error of the mean too small to visualize. Source data are provided as a Source Data file.