Figure 1.
Correlative studies suggest that pitavastatin reduces leukemia burden after a single dose in some patients. (A) Analysis of PBMCs from a patient with CLL. Left: the percentage of leukemia cells was determined by flow cytometry before treatment (baseline), after VEN ramp-up (VEN), and 24 hours after the first PIT dose (PIT 24 hours). Right: BH3 profiling was performed on gated CLL blasts by measuring cytochrome C release after exposure to DMSO alone, alamethicin (positive control apoptotic stimulus), PUMA2A (negative control peptide), or active BIM or PUMA peptides. The change in the percentage of cytochrome C–low cells between the VEN or PIT conditions and baseline was graphed as delta percentage priming. (B) Analysis of PBMCs from 2 patients with AML. The percentage of AML blasts was determined using flow cytometry. Each experiment in panels A and B was done with a single sample, without technical replicates. DMSO, dimethyl sulfoxide; PUMA, p53 upregulated modulator of apoptosis; BIM, BCL2 interacting mediator of cell dealth.

Correlative studies suggest that pitavastatin reduces leukemia burden after a single dose in some patients. (A) Analysis of PBMCs from a patient with CLL. Left: the percentage of leukemia cells was determined by flow cytometry before treatment (baseline), after VEN ramp-up (VEN), and 24 hours after the first PIT dose (PIT 24 hours). Right: BH3 profiling was performed on gated CLL blasts by measuring cytochrome C release after exposure to DMSO alone, alamethicin (positive control apoptotic stimulus), PUMA2A (negative control peptide), or active BIM or PUMA peptides. The change in the percentage of cytochrome C–low cells between the VEN or PIT conditions and baseline was graphed as delta percentage priming. (B) Analysis of PBMCs from 2 patients with AML. The percentage of AML blasts was determined using flow cytometry. Each experiment in panels A and B was done with a single sample, without technical replicates. DMSO, dimethyl sulfoxide; PUMA, p53 upregulated modulator of apoptosis; BIM, BCL2 interacting mediator of cell dealth.

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