Figure 2.
Somatic CNVs affecting MYC, MIR17HG, and PVT1 identified by WGS among DHITsig+ DLBCL tumors. Focal copy-number gains of MYC (A) or MIR17HG (B) identified among DHITsig+ DLBCL tumors. Red bars indicate regions where Control-FREEC identified a significant increase in copy number (P < .05). Compared with 162 GCB tumors without a MIR17HG amplification as determined by single-nucleotide polymorphism (SNP) arrays, expression of MIR17HG was significantly elevated among these 6 cases with MIR17HG copy gains (log2 fold change, 0.85; Wilcoxon P = .032). (C) The boundaries of focal PVT1 transcription start site (TSS) deletions identified in DHITsig+ tumors. *Indicates the PVT1 deletion identified in the double-minute chromosome.

Somatic CNVs affecting MYC, MIR17HG, and PVT1 identified by WGS among DHITsig+ DLBCL tumors. Focal copy-number gains of MYC (A) or MIR17HG (B) identified among DHITsig+ DLBCL tumors. Red bars indicate regions where Control-FREEC identified a significant increase in copy number (P < .05). Compared with 162 GCB tumors without a MIR17HG amplification as determined by single-nucleotide polymorphism (SNP) arrays, expression of MIR17HG was significantly elevated among these 6 cases with MIR17HG copy gains (log2 fold change, 0.85; Wilcoxon P = .032). (C) The boundaries of focal PVT1 transcription start site (TSS) deletions identified in DHITsig+ tumors. *Indicates the PVT1 deletion identified in the double-minute chromosome.

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