Figure 6
Effect of inhibition of c-Myc in primary cells on NKG2D ligand expression and NK-cell–mediated cytotoxicity. (A) Blasts from chemotherapy-resistant patients were isolated and incubated with c-Myc inhibitor for 24 hours and relative ULBP1/2/3 mRNA expression by real-time qPCR was measured and compared with nontreated blasts. (B) NK-cell–cytotoxicity of blasts with or without treatment with 10058-F4 at indicated E:T ratios. (C) Flow cytometric analysis of CD107a expression on NK cells cocultured for 4 hours in refractory blasts with or without inhibition of c-Myc with 10058-F4 (treatment of 24 hours, 100 µM) at E:T ratio of 10:1 (representative blot of n = 3). (D) Flow cytometric analysis for the expression of ULBP1/2/3 of AML refractory patients after treatment with c-Myc inhibitor for 24 hours.

Effect of inhibition of c-Myc in primary cells on NKG2D ligand expression and NK-cell–mediated cytotoxicity. (A) Blasts from chemotherapy-resistant patients were isolated and incubated with c-Myc inhibitor for 24 hours and relative ULBP1/2/3 mRNA expression by real-time qPCR was measured and compared with nontreated blasts. (B) NK-cellcytotoxicity of blasts with or without treatment with 10058-F4 at indicated E:T ratios. (C) Flow cytometric analysis of CD107a expression on NK cells cocultured for 4 hours in refractory blasts with or without inhibition of c-Myc with 10058-F4 (treatment of 24 hours, 100 µM) at E:T ratio of 10:1 (representative blot of n = 3). (D) Flow cytometric analysis for the expression of ULBP1/2/3 of AML refractory patients after treatment with c-Myc inhibitor for 24 hours.

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