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. 2015 Apr;100(4):e132–e136. doi: 10.3324/haematol.2014.112995

Figure 3.

Figure 3.

Trametinib (MEK inhibitor) and sorafenib (BRAF inhibitor) restored prednisolone sensitivity in RAS-mutant patients. (A1–G1) Sensitivity to 3.9 mg/mL prednisolone of 7 distinct pediatric BCP-ALL patients’ cell samples co-incubated with 2.5 mM trametinib (MEK1/2 inhibitor), sorafenib (BRAF inhibitor), AS1517499 (STAT6 inhibitor), Crizotinib (cMET inhibitor) or vehicle (DMSO) control measured in a 4-day MTT assay. Data are presented as mean+SEM of a duplicate experiment (t-test *P<0.05, **P<0.01, ***P<0.001). (A2–G2) Dose-response curve of prednisolone combined with the inhibitor giving the most prominent effect in A1–G1. Graphs represent 2.5 or 5.0 mM sorafenib (BRAF inhibitor), trametinib (MEK inhibitor) or vehicle control (DMSO). Data are presented as mean+SEM of a duplicate experiment (repeated measurement two-way ANOVA, interaction inhibitor, *prednisolone *P<0.05, **P<0.01, ***P<0.001). Sensitivity was corrected for cell death induced by the inhibitor/vehicle itself in the absence of prednisolone to facilitate assessment of pure prednisolone sensitizing effects. The upper 3 patients have RAS-mutations; the lower 4 patients are RAS-wild type.