Figure 2
Figure 2. Influence of caspase inhibitors on flavopiridol-mediated effects in CLL patient cells. (A) CD19+ CLL patient cells in media with 10% human serum were incubated with or without 1.5 μM FP for 6 hours in the presence or absence of 100 μM pan-caspase inhibitor (Z-VAD-fmk), caspase-8 inhibitor (Z-IETD-fmk), or caspase-9 inhibitor (Z-LEHD-fmk). CLL samples (N = 7) were analyzed for annexin binding as above. Data are shown relative to untreated cells, set at 100%. The effect of FP with Z-VAD-fmk was significantly less than with no inhibitor (*adjusted P < .001) as was the case with caspase-8 (**adjusted P = .04). The effect of FP with caspase-9 also tended to be less, although not significant (adjusted P = .08). (B) Samples (N = 8) were then assessed for mitochondrial membrane depolarization at 6 hours. Error bars represent plus or minus standard deviation. None of the caspase inhibitors blocked FP-mediated mitochondrial depolarization (adjusted P > .3 for each).

Influence of caspase inhibitors on flavopiridol-mediated effects in CLL patient cells. (A) CD19+ CLL patient cells in media with 10% human serum were incubated with or without 1.5 μM FP for 6 hours in the presence or absence of 100 μM pan-caspase inhibitor (Z-VAD-fmk), caspase-8 inhibitor (Z-IETD-fmk), or caspase-9 inhibitor (Z-LEHD-fmk). CLL samples (N = 7) were analyzed for annexin binding as above. Data are shown relative to untreated cells, set at 100%. The effect of FP with Z-VAD-fmk was significantly less than with no inhibitor (*adjusted P < .001) as was the case with caspase-8 (**adjusted P = .04). The effect of FP with caspase-9 also tended to be less, although not significant (adjusted P = .08). (B) Samples (N = 8) were then assessed for mitochondrial membrane depolarization at 6 hours. Error bars represent plus or minus standard deviation. None of the caspase inhibitors blocked FP-mediated mitochondrial depolarization (adjusted P > .3 for each).

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