Fig. 8

PLA therapy significantly reduces AraC resistance in primary AML cells ex vivo and in vivo. a Viability of primary cells from four AML patients after indicated treatments normalized to vehicle+AraC treatment for each patient sample (represented as a white bar and set to 1); other patient samples and combinations as well as normal CD34+ cells from healthy donors after indicated treatments are shown in Additional file 1: Figure S5I. b Viability and death of primary cells from AML mouse models driven by HoxA9/Meis1 and MLL-AF9 after indicated treatments. c–g Bioluminescence images and quantification of tumor growth in NSG mice engrafted with MOLM13 cells and at the indicated days after engraftment, were treated with PLA therapy or AraC (c, d) and in C57BL/6 mice engrafted with primary HoxA9-Meis1/luciferase cells and treated with PLA therapy or AraC with two different dosage schedules (8e: treated 8 times with drugs over 4 days versus 8f: 6 times with drugs over 2 weeks) or treated with PFD plus LY or vehicle as a control (g). h Kaplan-Meier survival curves of MLL-AF9 engrafted C57BL/6 mice, treated with PLA therapy or AraC. The number of drug injections in c–h is marked: 8X (c, e), 4X (d), 6X (f, g), and 12X (h). For c, e–g, relative luciferase activity was quantified and plotted as bar graphs to represent tumor survival. *p ≤ 0.05. Data are represented as average ± SEM. See also Additional file 1: Figures S5-S6