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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Leukemia. 2015 Apr 17;29(8):1702–1712. doi: 10.1038/leu.2015.99

Figure 5. High efficacy of targeting both MCL1 and BCL2 in a model of MYC-BCL2 double-hit lymphoma.

Figure 5

(a) Schematic for generation of MYC-BCL2 genetically defined tumors (see text). (b) Tumor onset was detected with palpation and blood smear evaluation and compared using Kaplan-Meier analysis. (c) Representative FACS plots for GFP fluorescence of partially infected HSCs initially transplanted compared to resulting lymphoma cells at disease onset. (d) Representative pathology samples of c-MYC vs. vector tumors, imaged with EVOS XL Cell Imaging System (Life Technologies). (e) Lymphoma cells from a primary VavP-Bcl2/c-MYC recipient animal were cultured ex vivo and exposed to dinaciclib, ABT-199, or the combination for 24 hours. Viability at 250 nM and CI vs. Fa. (mean of quadruplicates ± SEM.) (f) Tumor cells from two different primary VavP-Bcl2/c-MYC recipients were exposed to dinaciclib and blotted as in Figure 1b. (g) Kaplan-Meier overall survival analysis of VavP-Bcl2/c-MYC tumor-bearing animals following initiation of treatment as indicated. The log-rank test was used to calculate p values. NS: p ≥ 0.05. (h) Representative blood smears of Vavp-Bcl2/c-MYC tumor-bearing mice during treatment. Blood smears were collected 7 days after treatment initiation, and stained with Hema-Quik II Stain Solutions. Imaged on EVOS XL Cell Imaging System (Life Technologies), scale bars 100 μm.