HGBCL-DH-BCL2 experience elevated SHM across MYC partner loci. (A) Median mutation counts across recurrent MYC partner loci covered by the targeted capture sequencing assay. (B) Mutation counts per tumor within the IGH Eμ enhancer and TSS of each constant gene. IGHM was separated from Eμ using the boundary defined in supplemental Figure 6A. In panels A-B, HGBCL-DH-BCL2 was used as the reference group for FDR-corrected Wilcoxon tests to identify significant differences in mutation counts for each locus. (C) A row-normalized heat map showing expression levels of each IGH constant gene determined by RNAseq. Samples are ordered according to IGHM expression. The CSR track indicates whether each tumor was predicted to express a functional IGHM/D (no) or a different IGHC gene (yes). (D) Expression levels of genes that may be involved in the regulation of aSHM and/or CSR compared with pairwise FDR-corrected Wilcoxon tests. (E) Mutation counts at the MYC TSS stratified by lymphoma entity and MYC rearrangement partner or predicted IGH rearrangement mechanism. The number and percentage of tumors with ≥1 mutation in the MYC TSS are indicated above each grouping. Within each entity, FDR-corrected Wilcoxon tests were used to compare the mutation counts for each MYC-R partner/mechanism group (with at least 4 tumors) with that of IGH-CSR. ns, not significant; ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. IGHC, constant region of IGH locus; IGHVDJ, variable (V), diversity (D), and joining (J) region of the IGH locus; ND, not done; REF, reference group.