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. Author manuscript; available in PMC: 2018 Aug 8.
Published in final edited form as: Cell Rep. 2018 Jun 12;23(11):3127–3136. doi: 10.1016/j.celrep.2018.05.034

Figure 5. The Effect of a Combination of PARP1 and RAD52 Inhibitors against BRCA1-Deficient Primary AML Xenograft in NSG Mice and against BRCA1-Deficient Solid Tumor Growth in Nude Mice.

Figure 5

(A and B) NSG mice were inoculated i.v. with 106 BRCA1-deficient primary AML xenograft cells. One week later, the animals were treated with vehicle (Control), F79 aptamer (F79), talazoparib (Tala), or F79 + Tala (six mice per group) for 7 consecutive days.

(A) Representative plots of peripheral blood leukocyte (PBL) from treated mice; mean percentage ± SD of human CD45+ AML cells in peripheral blood leukocytes 3 weeks after leukemia injection; *p ≤ 0.005 and **p < 0.001 in comparison with Control and single-compound treatment, respectively, using Student’s t test.

(B) Kaplan-Meier survival curves.

(C and D) Nu/nu mice were inoculated s.c. with 106 BRCA1-deficient MDA-MB-436 cells (C) and BRCA1-proficient MDA-MB-436 +BRCA1 cells (D). Tumor-bearing animals were treated with D-I03, talazoparib (Tala), or D-I03+Tala for 7 consecutive days (three to five mice per group). Results represent mean ± SD fold increase of tumor volume; *p < 0.05 compared with individual agents.

See also Figures S5–S7 and Table S1.