Figure 4.
Figure 4. P-CrKL in CD34+CD38– CML cells treated with 5 μM IM, 10 nM, and 150 nM dasatinib. As described in Figure 3, CD34+CD38– CML cells were cultured with or without IM (5 μM), 10 or 150 nM dasatinib. CD34+CD38– CML cells treated with IM showed no significant inhibition of CrKL phosphorylation at either 16 or 72 hours. Dasatinib (10 nM)–treated CD34+CD38– CML cells showed a 26% reduction in P-CrKL at 16 hours, as compared to no-drug control (100%), which was not significantly different to IM-treated cells (P = .30). After 72 hours, the difference between IM and dasatinib 10 nM was significant (P = .001). CD34+CD38– CML cells treated with 150 nM dasatinib showed increasing inhibition of CrKL phosphorylation at 16 and 72 hours (–66% and –79% of control, respectively) (P = .007 and .005 versus dasatinib 10 nM and P = .004 and P < .001 versus IM 5 μM). Das indicates dasatinib.

P-CrKL in CD34+CD38 CML cells treated with 5 μM IM, 10 nM, and 150 nM dasatinib. As described in Figure 3, CD34+CD38 CML cells were cultured with or without IM (5 μM), 10 or 150 nM dasatinib. CD34+CD38 CML cells treated with IM showed no significant inhibition of CrKL phosphorylation at either 16 or 72 hours. Dasatinib (10 nM)–treated CD34+CD38 CML cells showed a 26% reduction in P-CrKL at 16 hours, as compared to no-drug control (100%), which was not significantly different to IM-treated cells (P = .30). After 72 hours, the difference between IM and dasatinib 10 nM was significant (P = .001). CD34+CD38 CML cells treated with 150 nM dasatinib showed increasing inhibition of CrKL phosphorylation at 16 and 72 hours (–66% and –79% of control, respectively) (P = .007 and .005 versus dasatinib 10 nM and P = .004 and P < .001 versus IM 5 μM). Das indicates dasatinib.

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