Reprogramming of KBM7 cells results in escape from oncogene addiction. (A) KBM7-iPSCs acquired insensitivity to treatment with 1μM of the BCR-ABL kinase inhibitor imatinib (Gleevec), whereas parental KBM7 cells were highly sensitive. KBM7 cells, reprogrammed KBM7-iPS2 cells, and nonhematopoietic differentiated derivatives were cultured without (top row) or with the addition of 1μM imatinib for 3 days (bottom row). All images were acquired with a standard Nikon microscope with a 10× objective. (B) Viability of KBM7 cells infected with retroviral constructs encoding indicated cDNAs on imatinib treatment 7 days after infection. Only when the 4 factors were expressed in combination, KBM7 cells acquired insensitivity to imatinib. Cell viability was measured using an XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) conversion assay. Values given are percentages of uninfected control cultures. Data are the mean plus or minus SD values from a typical experiment performed in triplicate. (C) Flow cytometry histograms of KBM7 cells 7 days after infection with retroviruses expressing indicated cDNAs showed that a combination of the 4 reprogramming factors led to loss of expression of CD45, a pan-hematopoietic marker. (D) Flow cytometric analysis of KBM7-iPSCs differentiated into the hematopoietic lineage showed distinct subpopulation stained by CD45 and CD43 antibodies. Imatinib treatment resulted in a reduction of these subpopulations.