Figure 3.
Figure 3. Rapamycin inhibits proliferation only of cells driven by the D816V c-kit mutation. (A) Evaluation of the ratio of GAC (Wt) to GTC (D816V) c-kit mutation in α-155, D816V-transfected α-155, and HMC-1 by direct sequencing of c-kit exon 17. (B) Rapamycin and imatinib sensitivities of cells containing different mutated c-kit, including HMC-1 (D816V; □), α-155 (V560G; dark gray columns), and D816V-transfected α-155 (▦), were assessed after 48 hours of culture. Histograms represent the percentage of cell proliferation. Data are means ± SD of 3 separate experiments each plated in triplicate. (C) Rapamycin sensitivity on cell proliferation of normal bone marrow–derived mast cells (BMMCs; left panel) and transgenic mice for human D816V-mutated c-kit (right panel) cultured in the presence of rapamycin (5 nM) for 96 to 192 hours. Data represent 1 of 3 separate experiments plated in triplicate.

Rapamycin inhibits proliferation only of cells driven by the D816V c-kit mutation. (A) Evaluation of the ratio of GAC (Wt) to GTC (D816V) c-kit mutation in α-155, D816V-transfected α-155, and HMC-1 by direct sequencing of c-kit exon 17. (B) Rapamycin and imatinib sensitivities of cells containing different mutated c-kit, including HMC-1 (D816V; □), α-155 (V560G; dark gray columns), and D816V-transfected α-155 (▦), were assessed after 48 hours of culture. Histograms represent the percentage of cell proliferation. Data are means ± SD of 3 separate experiments each plated in triplicate. (C) Rapamycin sensitivity on cell proliferation of normal bone marrow–derived mast cells (BMMCs; left panel) and transgenic mice for human D816V-mutated c-kit (right panel) cultured in the presence of rapamycin (5 nM) for 96 to 192 hours. Data represent 1 of 3 separate experiments plated in triplicate.

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