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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Leuk Res. 2014 Nov 11;39(1):65–71. doi: 10.1016/j.leukres.2014.10.009

Figure 6. PF potentiates bosutinib lethality in primary patient specimens including the T315I mutation but not in normal CD34+ cells.

Figure 6

(A) CD34+ cells from 5 patients with CML were exposed to PF (0.2–0.4 mol/L) or 0.1-1.2 mol/L bosutinib individually or in combination for 48-72 hr, after which the percentage of apoptotic cells was determined by annexin V/PI using flow cytometry, (* p<0.05, significantly greater than values for single-agent treatment). All samples were sequenced in the BCR/ABL kinase domain. (B) Cells from specimen #5 (clinically dasatinib-resistant), K562 cells, amd BaF3/T315I cells were exposed to dasatinib 25 -100 nmol/L for 48 hr, after which the percentage of apoptotic cells was determined as above. (C) Cells from specimen #5 were treated with PF (0.4 mol/L), bosutinib (1.2 mol/L) or in combination for 30 hr, after which cells were lysed and subjected to Western blot analysis. (D) Normal cord blood CD34+ cells were isolated and exposed to PF 0.4 mol/L and/or bosutinib at a concentration of 1.2 mol/L for 48 hr, after which the percentage of apoptotic cells was determined by annexin V/PI positivity using flow cytometry. p > 0.3 = not significantly different compared to values for either agent alone.