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

Fig. 4. Dual MDM2/XPO1 inhibition induces synergistic anti-leukemia effects in Ven-R AML cells.

Fig. 4.

(A) c-MYC protein levels in primary AML samples from patients sensitive to Ven-containing regimens (Ven-S; N = 6), those who had remission and then relapse (Ven-Rem/rel; N = 3), and those who had primarily refractory disease (Ven-Ref; N = 7). Data represent means ± SEM. (B) Immunoblot of c-MYC in MV4;11 Ven-S and resistant (Ven-R) cells. (C) Live cell numbers of MV4;11 Ven-S and Ven-R cells treated with Mil, Sel, or Mil + Sel for 72 hours. (D) Schematic diagram of in vivo xenograft model. (E) Images of leukemia burden measured by luciferin intensities in three representative mice from each treatment group. (F) Luciferin intensities of each treatment group (N = 8, 9, 8, 9, and 5 for vehicle, Ven, Mil, Sel, and Mil + Sel, respectively). (G) Survival curves of each treatment group and treatment durations of Mil (blue rectangle) and Sel (red arrows). (H) Immunoblots for c-MYC in MV4;11 Ven-R cells obtained from moribund mice in each in vivo treatment group. (I) Ven (48 hours)–specific annexin V induction in MV4;11 Ven-R cells after each in vivo treatment. (J) Live cell numbers of MV4;11 Ven-R cells treated with 200 nM of Ven (48 hours) with prior transfection with control siRNA (siCtrl) or MYC siRNA (siMYC) sequences. Histone H3 serves as the loading control in (B) and (H). **P < 0.01; ****P < 0.0001.