Fig. 4: Leukemia cells rely on IL-7R signaling, which boosts upon transformation.

a Immunoblot analysis of phosphorylated STAT5 and S6 levels in sorted pro+pre-B cells from control (n = 4) and pre-leukemic (n = 3) mice, IL-7-deprived for 12 h. Graphs represent densitometry values for P-STAT5 and P-S6 normalized to respective total protein. b Differential gene expression of known IL-7R signaling targets in pre-leukemia and leukemia samples compared to controls (reference category). Moderate t-test performed. c–e Differential expression of (c) STAT5, (d) MYC, and (e) mTOR targets in leukemia versus control samples. Significantly upregulated and downregulated genes (adj. p < 0.05; moderate t-test) are shown in red and in blue, respectively. f Immunoblot analysis of phosphorylated S6 levels in control (n = 3) and leukemia (n = 6) samples analyzed ex vivo. g Transcriptomic and proteomic gene set enrichment analysis (GSEA) showing a significant enrichment of the mTOR signaling hallmark gene set in leukemias versus controls. h Leukemia cells were cultured in the presence or absence of pharmacological inhibitors of JAK1/2 (INCB018424; ruxolitinib), STAT5 (STAT5 inhibitor), and PI3K (LY294002) at the indicated doses, and viability was evaluated at 48 and 72 h. Results from a representative mouse (n = 3). Lines represent average of duplicates that are shown. Source data are provided as a Source Data file.