Figure 3.
Activation of caspase-3. Activation in AR230-r1 cells exposed to the combinations of imatinib plus As2O3 (A) and imatinib plus decitabine (B) at resistant (1 μM) and sensitive (2 μM) doses of imatinib. AR230-r1 cells exposed to 1 μM imatinib show low-level activation of caspase-3 (C). Combination treatment with a second agent (CombTx) leads to fewer apoptotic cells than one would predict from the sum of single-agent treatment (Σ) in the presence of 1 μM imatinib (1 μM + 1 μM [A] or 1 μM + 0.5 μM [B]) but to more apoptosis than one would predict from single-agent treatment in the presence of 2 μM imatinib (2 μM + 1 μM [A] or 2 μM + 0.5 μM [B]). Differences were significant for imatinib plus As2O3 as determined by the t test (*P < .05), indicating synergy, whereas they were not significant for imatinib plus decitabine, indicating additivity. Columns represent means of 3 independent experiments ± SD.

Activation of caspase-3. Activation in AR230-r1 cells exposed to the combinations of imatinib plus As2O3 (A) and imatinib plus decitabine (B) at resistant (1 μM) and sensitive (2 μM) doses of imatinib. AR230-r1 cells exposed to 1 μM imatinib show low-level activation of caspase-3 (C). Combination treatment with a second agent (CombTx) leads to fewer apoptotic cells than one would predict from the sum of single-agent treatment (Σ) in the presence of 1 μM imatinib (1 μM + 1 μM [A] or 1 μM + 0.5 μM [B]) but to more apoptosis than one would predict from single-agent treatment in the presence of 2 μM imatinib (2 μM + 1 μM [A] or 2 μM + 0.5 μM [B]). Differences were significant for imatinib plus As2O3 as determined by the t test (*P < .05), indicating synergy, whereas they were not significant for imatinib plus decitabine, indicating additivity. Columns represent means of 3 independent experiments ± SD.

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