Figure 5.
WM subgroups show differential biological features. (A) Oncoprint of genomic aberrations in WM separated by methylation subtype. Epigenetic maturity (as defined in Figure 3) is indicated for each sample; bars below and above represent low and high maturity, respectively. Mutations were mostly clonal VAFs (black) with a minority of subclonal mutations observed (VAF <10%; dark gray). (B) The proportion of patients with IGHV1-6 rearrangements separated by methylation subtype. (C) Box plot of the mean fluorescence intensity of CD38 on WM tumor cells separated by methylation subtype, gated on CD19+ and monotypic light chain–restricted cells. (D) Summary of tumor cell morphology of WM patient BM samples. Percentages of cell types were averaged within WM methylation subtypes. n.s., not significant.

WM subgroups show differential biological features. (A) Oncoprint of genomic aberrations in WM separated by methylation subtype. Epigenetic maturity (as defined in Figure 3) is indicated for each sample; bars below and above represent low and high maturity, respectively. Mutations were mostly clonal VAFs (black) with a minority of subclonal mutations observed (VAF <10%; dark gray). (B) The proportion of patients with IGHV1-6 rearrangements separated by methylation subtype. (C) Box plot of the mean fluorescence intensity of CD38 on WM tumor cells separated by methylation subtype, gated on CD19+ and monotypic light chain–restricted cells. (D) Summary of tumor cell morphology of WM patient BM samples. Percentages of cell types were averaged within WM methylation subtypes. n.s., not significant.

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