Hypoxia-responsive genes are up-regulated in LSCs. BCR-ABL–expressing LSK cells and control LSK cells were sorted from mice receiving BCR-ABL or empty vector-transduced BM cells for DNA microarray analysis. (A) The heatmap compares the activation of the HIF1α signaling pathway in BCR-ABL–expressing LSK cells and control LSK cells. (B) Gene set enrichment analysis (GSEA) displays the expression profiling of HIF1α targets in BCR-ABL–expressing LSK cells (P < .001). (C) Microarray data showed higher expression of HIF1α, vascular endothelial growth factor (VEGF), glucose transporter type 1 (GLUT1), and transforming growth factor α (TGFα) in BCR-ABL–expressing LSK cells comparing to normal LSK cells. (D) Real-time RT-PCR was performed with primers specific for HIF1α, VEGF, GLUT1, TGFα, and PGK1. The results were normalized using actin as a control, and shown as mean ± SD. *P < .05; **P < .01.