Figure 3.
Overexpression of HOXA10-AS promotes leukemic growth and perturbs differentiation. (A) Percentage of LBid-HOXA10-AS–transduced GFP+ patient-derived blasts normalized to day 2 and to LBid-ctrl-transduced cells (n = 3; 2-way variance analysis; presented as mean ± SD; **P < .01). (B) Percentage of LBid-HOXA10-AS-transduced GFP+ ML-2 cells normalized to day 2 and to LBid-control–transduced cells in the presence of 1 µM BMS-345541 or dimethyl sulfoxide (n = 3; 2-way variance analysis; presented as mean ± SD; **P < .01). (C) FACS analysis of CD11b+/CD14+ and CD14+/CD163+ cells on day 11 of in vitro monocytic differentiation in the presence or absence of 1 µM BMS-345541 (n = 3-9; 2-way variance analysis; presented as mean ± SD). (D) May-Grünwald-Giemsa staining on day 10 of monocytic differentiation (original magnification ×400). (E) Number of CFUs in methylcellulose-based colony-forming assays (n = 4; 2-way variance analysis; presented as mean ± SD; **P < .01).

Overexpression of HOXA10-AS promotes leukemic growth and perturbs differentiation. (A) Percentage of LBid-HOXA10-AS–transduced GFP+ patient-derived blasts normalized to day 2 and to LBid-ctrl-transduced cells (n = 3; 2-way variance analysis; presented as mean ± SD; **P < .01). (B) Percentage of LBid-HOXA10-AS-transduced GFP+ ML-2 cells normalized to day 2 and to LBid-control–transduced cells in the presence of 1 µM BMS-345541 or dimethyl sulfoxide (n = 3; 2-way variance analysis; presented as mean ± SD; **P < .01). (C) FACS analysis of CD11b+/CD14+ and CD14+/CD163+ cells on day 11 of in vitro monocytic differentiation in the presence or absence of 1 µM BMS-345541 (n = 3-9; 2-way variance analysis; presented as mean ± SD). (D) May-Grünwald-Giemsa staining on day 10 of monocytic differentiation (original magnification ×400). (E) Number of CFUs in methylcellulose-based colony-forming assays (n = 4; 2-way variance analysis; presented as mean ± SD; **P < .01).

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