Bryostatin-1 and hispidin rescue BMS-214662–induced apoptosis. (A) Decrease in E2F1 and increased phosphorylation of Cdk2 mediated by BMS-214662 were modulated by 100nM bryostatin-1 as shown by Western blotting analysis (n = 3). (B) Conformational changes of Bax were measured by FACS in CML cells after addition of 250nM BMS-214662, 100nM bryostatin-1, or combination for 24 hours (n = 3). (C) CD34⁺ CML cells were treated as in panel A (top panel) or with 250nM BMS-214662, 5μM hispidin (bottom panel), or combination for 24 hours and loss of MOMP was measured (n = 3). (D) Cells were treated as indicated and observed under phase-contrast microscope. (E) Bcl2 phosphorylation was analyzed by FACS in CD34⁺ CML cells after treatment with no drug or 250nM BMS-214662 or cotreatment with BMS-214662 and 100nM bryostatin-1 for 24 hours (n = 3). (F) Activation of caspase-3 was measured in CML CD34⁺ cells after treatment with 250nM BMS-214662, 100nM bryostatin-1, or 5μM hispidin or cotreatment (n = 5). Activation of caspase-3 was also measured in CD34⁺38⁻ and CD34⁺38⁺ CML cells after treatment with 250nM BMS-214662, 100nM bryostatin-1, and 5μM hispidin (n = 2). Error bars represent ± SD. *P < .05.