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. 2023 Nov 29;9(48):eadh1436. doi: 10.1126/sciadv.adh1436

Fig. 5. MDM2/XPO1 inhibition leaves alive p21high/Ki-67low AML cells and triple inhibition of MDM2, XPO1 and BCL2 exhibits superior anti-leukemia effects in Ven-R AML cells.

Fig. 5.

(A) Uniform manifold approximation and projection (UMAP) data of target protein levels determined in OCI-AML3 cells with indicated treatments (160 nM of Mil and/or Sel, 48 hours). Top: Two major populations of live (left) and dead (right) cells under each treatment condition. Bottom: Protein levels on a color scale with residual AML cells after Mil + Sel highlighted in connected red rectangles. (B) Schematic of the in vivo PDX AML model. (C) Percentages of live human AML cell numbers in PB specimens from mice treated with the indicated drugs. (D) OS of mice with indicated treatments (N = 8, 8, 8, 5, 7, 7, 8, and 8 for vehicle, Ven, Mil, Sel, Mil + Sel, Mil + Ven, Sel + Ven. and Mil + Sel + Ven groups, respectively). (E) Murine platelet counts in PB specimens in each treatment group at week of 7. (F) Murine CD45+ cell numbers in PB specimens collected from indicated treatment groups over the entire treatment courses (N = 6). Data represent means ± SEM values in (C), (E), and (F). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.