Figure 7.
Figure 7. Comparison of imatinib treatment with functional inhibition of c-kit signaling. Mobilized CD34+ cells from healthy donors were expanded in SFM supplemented with human growth factor starting with 1 × 103 cells/well under increasing doses of imatinib (0-10 μM) either with or without SCF or with or without the addition of a monoclonal antibody that blocks SCF-dependent dimerization of c-kit. The mean ± SE of 3 individual donors after 12 days in culture is shown. The asterisk (*) denotes significant differences in imatinib-treated as compared to untreated control cells (▪) for each condition. Note that no significant difference was observed between untreated cells that either did not receive SCF or where c-kit signaling was functionally blocked by the addition of a monoclonal anti–c-kit antibody. Effect of treatment with imatinib was significantly more pronounced than the effect achieved by functional c-kit inhibition alone (P < .001).

Comparison of imatinib treatment with functional inhibition of c-kit signaling. Mobilized CD34+ cells from healthy donors were expanded in SFM supplemented with human growth factor starting with 1 × 103 cells/well under increasing doses of imatinib (0-10 μM) either with or without SCF or with or without the addition of a monoclonal antibody that blocks SCF-dependent dimerization of c-kit. The mean ± SE of 3 individual donors after 12 days in culture is shown. The asterisk (*) denotes significant differences in imatinib-treated as compared to untreated control cells (▪) for each condition. Note that no significant difference was observed between untreated cells that either did not receive SCF or where c-kit signaling was functionally blocked by the addition of a monoclonal anti–c-kit antibody. Effect of treatment with imatinib was significantly more pronounced than the effect achieved by functional c-kit inhibition alone (P < .001).

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