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. Author manuscript; available in PMC: 2016 Dec 15.
Published in final edited form as: Cell Rep. 2015 Nov 25;13(10):2159–2173. doi: 10.1016/j.celrep.2015.10.073

Figure 5. Dependence of AML Signaling Networks on teHsp90 Is Conserved at the Leukemic Progenitor and Stem Cell Level.

Figure 5

(A) Percent annexin-V-positive leukemia stem cells (LSCs) and lymphocytes in primary AML specimens treated with 500 nM PU-H71 for 48 hr. Each color represents an individual sample.

(B) Correlation between p-STAT5 (y axis) and sensitivity of LSCs to PU-H71 (x axis).

(C) Percent colony-forming units (CFUs) relative to untreated control (UT) for primary AML cells or CD34+ cord blood (CB) after 48 hr treatment with 500 nM PU-H71. Myeloid colonies are shown for normal CB cells.

(D) Schematic representation for the ex vivo engraftment assay to evaluate the effect of PU-H71 treatment on the ability of LSCs to initiate disease in immunodeficient mice.

(E and F) Percent engraftment of human AML cells (E) and CD34+ CB cells from two units (CBa and CBb) (F) after ex vivo treatment with PU-H71 for 24 hr. Each symbol represents an individual mouse.

Values denote mean ± SEM.