Decrease in tumor burden with A-PAC in vivo treatment and the role of NF-κB in A-PAC–induced cell death. (A) Percent engraftment of AML 9 at 6 weeks posttransplant and 3 weeks after intraperitoneal treatments (A-PACs or phosphate-buffered saline 2 times/week for 3 weeks or with 60 mg/kg Ara-C daily for 5 days). Percent leukemia burden is shown for the indicated treatments. Data represented as mean ± SEM and significant if *P < .05; *P = .0332 (1-way analysis of variance). (B) Pan-caspase inhibitor Z-VAD (20 µM) cannot rescue AML cells from A-PAC (250 μg/mL) cell death. (C) NF-κB gene family upregulation and cell death after 4 hours with A-PACs (62.5 μg/mL; 31.25 μg/mL for Ramos). Cell lines from left to right: MV4-11 (green), K562 (red), REH (brown), MOLM-13 (purple), SKNO-1 (blue), Ramos (gray). (D) NF-κB activation after 4 hours of A-PAC treatment in MOLM-13; positive control is 2.5 μg Jurkat (TPA+CI) nuclear extract. (E) A-PAC cell death after pretreatment with NF-κB inhibitor SN50 (100 µg/mL) in 2 cell lines and a primary AML sample (blue arrows indicate line for LD₅₀); shown with log concentration (µg/mL). (F) SN50 increased the ability of parthenolide (PTL) to induce cell death in a primary AML10 cells; shown with log concentration (µM). (G) Activation of NF-κB after 4 hours of treatment with A-PACs (32.25 μg/mL) or PTL (5 μM) with and without SN50 (36 μM) in AML10 cells. Data mean ± SEM were significant if *P < .05, **P < .0 1, ***P < .001 (Student t test, with the exception of panel A). OD, optical density.