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. Author manuscript; available in PMC: 2018 Oct 1.
Published in final edited form as: Mol Cancer Ther. 2017 Jul 17;16(10):2069–2082. doi: 10.1158/1535-7163.MCT-17-0141

Figure 4.

Figure 4.

Overexpression of cMYC results in resistance to CAL-130 and GSI treatments. A-D, FACS dot plots (A and B) and viability bar graphs (C and D) of a representative CD2-Lmo2-driven T-ALL cell line (03007) transfected with mCherry-expressing empty or WT cMYC vector and treated with CAL-130 (72 hours), CompE (27, 96 and 120 hours) or DMSO control. Data represent mean ± SEM (***, P < 0.0001; n = 3, t test). cMYC protein expression in the same cells treated with CAL-130 (E) or CompE (F) for 24 and 48 hours, respectively. G, Flow cytometric analysis of disease status in two representative (n = 5) Gt(ROSA)26Sortm13(CAG-MYC, -CD2*)Rsky/J; Lck-cre/Pten(fl/fl) mice immediately before and 7 days after initiating treatment with dual PI3Kγ/δ inhibitor CAL-130 (10 mg/kg every 8h) for 7 days. Tumor drug response was determined by assessing for changes in circulating blasts (Thy1.2+/Ki67+) and propidium iodide (PI)-staining.