Pharmaceutical inhibition of PI3Kγ suppresses the progression of AML. (A) Representative images of colony formation of mouse BM MLL-AF9⁺ AML cells upon 1 μM IPI-549 treatment. Scale bar, 20 μm. (B-C) Colony numbers (B) and derived total cell counts (C) of mouse BM AML cells upon 1 μM IPI-549 treatment were calculated (n = 3). (D-E) The frequencies of leukemia cells in the PB (D, n = 6) and overall survival (E, n = 6) were compared among the recipients transplanted with mouse MLL-AF9⁺ AML cells, followed by 15 mg/kg IPI-549 treatment starting at 2 weeks after transplantation. (F-G) The percentages of human CD45⁺ AML cells in the PB (F, n = 6) and the overall survival (G, n = 6) were compared in the recipients transplanted with PDX1 cells, followed by 15 mg/kg IPI-549 treatment starting at 2 weeks after transplantation. (H-I) The percentages of human CD45⁺ AML cells in the PB (H, n = 6) and the overall survival (I, n = 6) were compared in the recipients transplanted with PDX2 cells, followed by 15 mg/kg IPI-549 treatment starting at 2 weeks after transplantation. (J-K) The percentages of human CD45⁺ AML cells in the PB (J, n = 6) and the overall survival (K, n = 6) were compared in the recipients transplanted with PDX3 cells, followed by 15 mg/kg IPI-549 treatment starting at 2 weeks after transplantation. (L-S) Primary AML patient cells were treated with 5 μM IPI-549. Cell number was calculated at the indicated time points (n = 3). (T-U) Colony numbers (T) and derived total cell counts (U) of primary AML patient cells upon 5 μM IPI-549 treatment were calculated (n = 3). (V) Working model for the functions of PIK3CG in leukemogenesis (PI3Kγi: PI3Kγ inhibitor). Data are represented as mean ± SEM. Student 2-tailed unpaired t test for panels B-D,F,H,J,L-U and log-rank test for panels E,G,I,K were used for the comparison of statistical significance. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001.