mTOR inhibitors synergize with 17-AAG to promote leukemia cell death. (A) Jurkat cells were treated with vehicle (Ctrl), 100nM rapamycin (Rapa), 5μM 17-AAG, or rapamycin (Rapa) plus 17-AAG for 0, 24, or 48 hours. The relative change in the number of viable cells at each time point was determined by a trypan blue exclusion assay. The total number of viable cells at 0 hours was set at 1. The data shown are the average of triplicate samples from 1 of 3 independent experiments. (B) Jurkat cells were treated with vehicle, 400nM pp242 (+pp242), or pp242 plus 5μM 17-AAG for 0, 24, or 48 hours. The relative change in the number of viable cells at each time point was determined by a trypan blue exclusion assay. The total number of viable cells at 0 hours was set at 1. The data shown are the average of duplicate samples from 1 of 2 independent experiments. (C) Wild-type p210 BCR-Abl mouse pre-B leukemia cells were treated with vehicle, 100nM rapamycin (Rapa), 5μM 17-AAG, or rapamycin (Rapa) plus 17-AAG for 0, 24, or 48 hours. The relative change in the number of viable cells at each time point was determined by a trypan blue exclusion assay. The total number of viable cells at 0 hours was set at 1. The data shown are the average of triplicate samples from 1 of 3 independent experiments. (D) Wild-type p210 BCR-Abl pre-B leukemia cells were treated with vehicle, 400nM pp242 (pp242), or pp242 plus 5μM 17-AAG for 0, 24, or 48 hours. The relative change in the number of viable cells at each time point was determined by a trypan blue exclusion assay. The total number of viable cells at 0 hours was set at 1. The data shown are the average of duplicate samples from 1 of 3 independent experiments.