Hypoxia induces HIF1-α expression in CML progenitors that can be partially attenuated by imatinib. (A) Representative immunohistochemical staining for HIF1-α and HIF2-α proteins in normal, CP, and BC CML BM specimens. (B) Immunofluorescence detection of HIF1-α protein expression in CD34⁺CD38⁻ and CD34⁺CD38⁺ populations. Results show representative images of 4 independent experiments. Scale bars represent 10 µm. (C) The levels of HIF1-α, pBCR-ABL1, pSTAT5, and pCrkL in CD34⁺ CML samples were detected by western blotting. Representative images of 2 independent experiments are shown. (D) The expression of HIF1-α, hypoxia-regulated genes (BNIP3, VEGFA, ALDOC, and GLUT1), and the BCR-ABL1-regulated gene WT1 in CD34⁺CD38⁻ and CD34⁺CD38⁻ subpopulations is shown. Expression was quantified by real-time quantitative polymerase chain reaction after normalization against the housekeeping gene, TBP (n = 3). Red bars highlight genes induced by hypoxia and downregulated by concurrent imatinib treatment.