Figure 6.
Figure 6. Combined ATRA/As treatment overcomes FLT3-ITD-triggered resistance. (A) GSEA analysis for 50 hallmark gene sets between P/R and P/R-FLT3ki mice treated during 9 or 24 hours with ATRA/As. Only significant pathways were represented (with FDR.q.val <0.05) according to NES value. (B) GSEA analysis of the p53 pathway in P/R and P/R-FLT3ki mice treated during 9 or 24 hours with ATRA/As. NES and FDR are noted. FDR.q.val <0.05 are in bold. (C) Survival of secondary recipients transplanted with APL bone marrow cells from ATRA/As 6-day-treated primary APL mice in both models (n ≥ 8 for each model). (D) Comparison of spleen weight (left), differentiation (CD11+/Gr1+, middle) and blast clearance (GFP+, right) of untreated (UT) or As 7-day-treated APL mice with MRP8-PML/RARAC212S in Pml+/+ or Pml−/− genetic background. Data are expressed as mean ± standard deviation of at least 2 independent experiments.

Combined ATRA/As treatment overcomes FLT3-ITD-triggered resistance. (A) GSEA analysis for 50 hallmark gene sets between P/R and P/R-FLT3ki mice treated during 9 or 24 hours with ATRA/As. Only significant pathways were represented (with FDR.q.val <0.05) according to NES value. (B) GSEA analysis of the p53 pathway in P/R and P/R-FLT3ki mice treated during 9 or 24 hours with ATRA/As. NES and FDR are noted. FDR.q.val <0.05 are in bold. (C) Survival of secondary recipients transplanted with APL bone marrow cells from ATRA/As 6-day-treated primary APL mice in both models (n ≥ 8 for each model). (D) Comparison of spleen weight (left), differentiation (CD11+/Gr1+, middle) and blast clearance (GFP+, right) of untreated (UT) or As 7-day-treated APL mice with MRP8-PML/RARAC212S in Pml+/+ or Pml−/− genetic background. Data are expressed as mean ± standard deviation of at least 2 independent experiments.

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