Figure 3.
Chemical inhibition of DUSP1 by BCI is ineffective. (A-C) Mice that received transplantation with wild-type Kit+ cells expressing CSF3RT618I. Graphs showing the total WBC levels (A), survival (B), and percent venus-positive cells as a surrogate leukemic burden (C). (D-F) Leukemic progression in mice that received transplantation with CSF3RT618I/Q741∗ expressing Kit+ cells. Graphs showing the total WBC levels (D), survival (E), and percent venus-positive cells as a surrogate leukemic burden (F). Dotted lines represent normal WBC levels. Treatment with BCI alone or with ruxolitinib is ineffective in suppressing the disease in both models of CSF3R induced leukemia. Representative data are from 2 independent experiments (3 mice per group), shown as the means ± SD. ∗P < .05; ∗∗P < .01; and ∗∗∗P < .001.

Chemical inhibition of DUSP1 by BCI is ineffective. (A-C) Mice that received transplantation with wild-type Kit+ cells expressing CSF3RT618I. Graphs showing the total WBC levels (A), survival (B), and percent venus-positive cells as a surrogate leukemic burden (C). (D-F) Leukemic progression in mice that received transplantation with CSF3RT618I/Q741∗ expressing Kit+ cells. Graphs showing the total WBC levels (D), survival (E), and percent venus-positive cells as a surrogate leukemic burden (F). Dotted lines represent normal WBC levels. Treatment with BCI alone or with ruxolitinib is ineffective in suppressing the disease in both models of CSF3R induced leukemia. Representative data are from 2 independent experiments (3 mice per group), shown as the means ± SD. ∗P < .05; ∗∗P < .01; and ∗∗∗P < .001.

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