Figure 1.

SFKs are constitutively activated in AML stem and progenitor cells independent of the cytogenetic risk. (A) Flow cytometry analysis of SFKs using a phosphospecific antibody recognizing the activated form of SFK members (Y416) in normal (Nml) or AML stem/primitive cells Lin⁻CD34⁺CD38^dim/−, AML progenitors cells Lin⁻CD34⁺CD38⁺, and AML more mature cells Lin⁻CD34⁻CD38⁻. Scatter plots comparing SFK phosphorylation (expressed as ratio of median fluorescence intensity for pSFK vs isotype control) in LinCD34⁺CD38^dim/−, Lin⁻CD34⁺CD38⁺, and Lin⁻CD34⁻CD38⁻ cells from AML (n = 56) and normal samples (n = 12; 3 BM, 4 CB, and 5 PBSC samples; ***P < .002). (B) Scatter plots comparing SFK phosphorylation in primary AML patients according to their prognostic risk category (bad, intermediate, and good prognosis). ns, non significant. (C) Western blots analysis for fresh or thawed CD34⁺ AML samples. Indicated antibodies are listed, and β-actin was used as a loading control. Results shown are representative of 9 AML samples analyzed.