Extended Data Fig. 8: Ruxolitinib treatment abrogates the effect of the combo treatment in primary AML samples. | Nature

Extended Data Fig. 8: Ruxolitinib treatment abrogates the effect of the combo treatment in primary AML samples.

From: Perturbing LSD1 and WNT rewires transcription to synergistically induce AML differentiation

Extended Data Fig. 8

a, Quantification of colonies formed by a primary AML sample (6998) treated with DMSO, GSK-LSD1 (50 nM), LY2090314 (100 nM) or combination of both inhibitors in the presence or absence of ruxolitinib. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). b, Analysis of IRF7, ISG15, MX1 and DDX58 mRNA relative levels in the primary sample (6998) treated with indicated inhibitors in the presence or absence of ruxolitinib. Values were normalized against GAPDH. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). c, Analysis of CD11b mRNA relative levels in the primary sample (6998) treated with the indicated inhibitors in the presence or absence of ruxolitinib. Values were normalized against GAPDH. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). d, Representative images of the AML primary sample (6998) treated with indicated inhibitors in the presence or absence of ruxolitinib and stained with Wright-Giemsa. Scale bars, 25 μm. The experiment was repeated three times with similar results. e, Quantification of colonies formed by a primary AML sample (6349) treated with DMSO, GSK-LSD1 (50 nM), LY2090314 (100 nM) and combination of both inhibitors in the presence or absence of ruxolitinib. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). f, Analysis of IRF7, ISG15, MX1 and DDX58 mRNA relative levels in the primary sample (6349) treated with indicated inhibitors in the presence or absence of ruxolitinib. Values were normalized against GAPDH. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). g, Analysis of CD11b mRNA relative levels in the primary sample (6349) treated with the indicated inhibitors in the presence or absence of ruxolitinib. Values were normalized against GAPDH. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). h, Representative images of the AML primary sample (6349) treated with indicated inhibitors in the presence or absence of ruxolitinib and stained with Wright-Giemsa. Scale bars, 25 μm. P-values were determined using two-way analysis of variance (ANOVA). The experiment was repeated three times with similar results. i, Analysis of CD11b mRNA relative levels in CD34+ cells treated with the indicated inhibitors. Values were normalized against GAPDH. Data are presented as mean ± SD of 3 biological independent experiments (n = 3). P-values were determined using two-way analysis of variance (ANOVA). “ns” indicates not significant. j, Morphology of CD34+ cells and their colonies treated with indicated inhibitors. Scale bars, 50 μm for colonies morphology and 25 μm for morphology of cells. The experiment was repeated three times with similar results.

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