Figure 6.
Combination of TCZ and ruxolitinib synergistically inhibits CFU-Mk generation from CALR- and JAK2V617F-mutated patients. (A-B) CD34+ isolated from CALR-mutated (n = 4) and JAK2V617F-mutated (n = 5) patients, respectively, were plated in IL-6–free clonogenic assays for CFU-Mk generation. Ruxolitinib (Ruxo; at a suboptimal dose of 5 nM) and TCZ (at 5 and 50 ng/mL) were added at the initiation of culture, and CFU-Mks were counted on day 12. Data are shown as percent number of colonies to control cultures in the absence of either drug. The isobologram for IC50 of TCZ and ruxolitinib to inhibiting CFU-Mk generation in CALRmut (C) and JAK2V617Fmut (D) patients was calculated according to the Chou and Talalay formula. All P values were determined by the Student t test (*P < .05; **P < .01; ***P < .001).

Combination of TCZ and ruxolitinib synergistically inhibits CFU-Mk generation from CALR- and JAK2V617F-mutated patients. (A-B) CD34+ isolated from CALR-mutated (n = 4) and JAK2V617F-mutated (n = 5) patients, respectively, were plated in IL-6–free clonogenic assays for CFU-Mk generation. Ruxolitinib (Ruxo; at a suboptimal dose of 5 nM) and TCZ (at 5 and 50 ng/mL) were added at the initiation of culture, and CFU-Mks were counted on day 12. Data are shown as percent number of colonies to control cultures in the absence of either drug. The isobologram for IC50 of TCZ and ruxolitinib to inhibiting CFU-Mk generation in CALRmut (C) and JAK2V617Fmut (D) patients was calculated according to the Chou and Talalay formula. All P values were determined by the Student t test (*P < .05; **P < .01; ***P < .001).

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