Fig. 6.
Fig. 6. P-gp+ve cells treated with caspase-dependent apoptotic stimuli retain proliferative and colony-forming ability. CCRF (A, C) and A7+ (B, D) cells (4 × 104 cells/mL) were treated with anti-Fas MoAb (0.01 mg/mL) (A, B) for 16 hours, or with recombinant soluble TNF (0.2 ng/mL) (C, D) for 48 hours. Cells were assayed for colony-forming ability by plating out 5 μL of cells in soft agar and incubating at 37°C for 12 days. In some wells, cells were preincubated for 30 minutes with 20 μmol/L ZVAD-fmk or control ZFA-fmk inhibitor and/or anti–P-gp MoAb MRK 16 (50 μg/mL) as indicated in Table 1. Data are calculated as the mean ± SE of triplicate plates and are representative of at least two different experiments.

P-gp+ve cells treated with caspase-dependent apoptotic stimuli retain proliferative and colony-forming ability. CCRF (A, C) and A7+ (B, D) cells (4 × 104 cells/mL) were treated with anti-Fas MoAb (0.01 mg/mL) (A, B) for 16 hours, or with recombinant soluble TNF (0.2 ng/mL) (C, D) for 48 hours. Cells were assayed for colony-forming ability by plating out 5 μL of cells in soft agar and incubating at 37°C for 12 days. In some wells, cells were preincubated for 30 minutes with 20 μmol/L ZVAD-fmk or control ZFA-fmk inhibitor and/or anti–P-gp MoAb MRK 16 (50 μg/mL) as indicated in Table 1. Data are calculated as the mean ± SE of triplicate plates and are representative of at least two different experiments.

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