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. Author manuscript; available in PMC: 2023 Jul 25.
Published in final edited form as: Oncogene. 2023 Apr 8;42(21):1751–1762. doi: 10.1038/s41388-023-02684-9

Figure 3. Copy number variation (CNV) analysis stratifies VQ cells based on recurrent amplification of chromosome 3 and monosomy chromosome 5.

Figure 3.

(A-B) CNV analysis was performed using the whole exome sequencing data as described in Materials and Methods. Orange dots indicate significant changes in log2 copy ratio for a given call segment in plasma cells compared to non-leukemia control samples. Location and name of tumor suppressors and oncogenes related to myeloma pathogenesis are shown in red. CNV plots are grouped according to recurrent CNV status. (C-F) Transcript levels of Nras (C), Fam46c (D), Cdk6 and Cdk4 (E), and Mmset/Whsc1 (F) are shown in CD138+ B220− cells from control and VQ recipient mice. FPKM, Fragments Per Kilobase of transcript per Million mapped reads. One-way analysis of variance with Tukey’s post-test was performed. Tissue of origin for individual samples is denoted by legend. (G-H) CD45.1 recipient mice were sub-lethally irradiated and injected with bone marrow cells from moribund VQ-D1 donor mouse or splenocytes from moribund VQ-D2 donor mouse. Six weeks (VQ-D1) or two weeks (VQ-D2) post-transplant, mice were treated with vehicle or trametinib. (G) Serum protein electrophoresis was performed to quantify the γ-globulin/Albumin (G/A) ratios in VQ-D1 and VQ-D2 recipient mice at day 21 of treatment. Two-sided t-test was performed. (H) Kaplan-Meier survival curves were plotted against days after treatment. Log-rank test was performed. Note: VQ-D1 results are combined from historical [24, 25] and new data. ns, not significant. *, p<0.05. **, p<0.01. ***, p<0.001. ****, p<0.0001.