Figure 1
Figure 1. Inhibition of primitive and committed progenitor growth after exposure to SKI-606. CD34+ cells from CML patients or healthy donors were exposed to SKI-606 or imatinib at the concentrations indicated for 96 hours. Cells were then assayed for primitive progenitors (LTC-IC) or committed progenitors (CFC) as described in “Progenitor assays.” (A,B) The effects of SKI-606 and imatinib on CML and normal primitive progenitor growth, respectively. (C,D) The effects on CML and normal committed progenitor growth, respectively. The percentage inhibition of primitive and committed progenitor growth after SKI-606 and imatinib treatment relative to untreated controls is shown. Results represent the mean plus or minus SEM based on replicate experiments (CML, n = 4; normal n = 3). (A-D) Concentrations of imatinib resulting in significant CML or normal progenitor growth suppression compared with untreated controls (†††P < .001; ††P < .01; †P < .05). Concentrations of SKI-606 inducing significant CML or normal progenitor growth suppression compared with untreated controls (***P < .001; **P < .01; *P < .05). (E) Inhibition of CML committed progenitor growth after exposure to SKI-606 (0.5 μM) and imatinib (5 μM) in combination (n = 3). The percentage of growth inhibition compared with untreated controls is shown for each condition. Significant suppression of progenitor growth in treated cells compared with controls (ns, not significant; ***P < .001; **P < .01; *P < .05). Error bars represent SEM.

Inhibition of primitive and committed progenitor growth after exposure to SKI-606. CD34+ cells from CML patients or healthy donors were exposed to SKI-606 or imatinib at the concentrations indicated for 96 hours. Cells were then assayed for primitive progenitors (LTC-IC) or committed progenitors (CFC) as described in “Progenitor assays.” (A,B) The effects of SKI-606 and imatinib on CML and normal primitive progenitor growth, respectively. (C,D) The effects on CML and normal committed progenitor growth, respectively. The percentage inhibition of primitive and committed progenitor growth after SKI-606 and imatinib treatment relative to untreated controls is shown. Results represent the mean plus or minus SEM based on replicate experiments (CML, n = 4; normal n = 3). (A-D) Concentrations of imatinib resulting in significant CML or normal progenitor growth suppression compared with untreated controls (†††P < .001; ††P < .01; †P < .05). Concentrations of SKI-606 inducing significant CML or normal progenitor growth suppression compared with untreated controls (***P < .001; **P < .01; *P < .05). (E) Inhibition of CML committed progenitor growth after exposure to SKI-606 (0.5 μM) and imatinib (5 μM) in combination (n = 3). The percentage of growth inhibition compared with untreated controls is shown for each condition. Significant suppression of progenitor growth in treated cells compared with controls (ns, not significant; ***P < .001; **P < .01; *P < .05). Error bars represent SEM.

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