ANXA5 deficiency in the BMM results in acceleration of MLL-AF9⁺ AML. (A) Schematic representation (left) of the murine retroviral transduction/transplantation model used to induce AML in WT and ANXA5-deficient mice. Kaplan-Meier style survival curve (right) of WT (red) or ANXA5-deficient (blue) recipient mice with MLL-AF9–induced AML (P = .003, log-rank test; n = 8). Median survival for WT mice was 63.5 days and for ANXA5-deficient mice was 55 days. Mice were irradiated with 2 × 450 cGy, and 5 × 10⁵ 5-fluorouracil (5-FU)–pretreated BM cells, transduced with MLL-AF9–expressing retrovirus, had been transplanted. (B) Kaplan-Meier style survival curve of WT (red) or ANXA5-deficient (blue recipient mice with MN1-induced AML (log-rank test, n = 9-10). Median survival for WT mice was 43 days and for ANXA5-deficient mice was 47 days. Mice were irradiated with 2 × 450 cGy, and 5 × 10⁵ 5-fluorouracil–pretreated BM cells, transduced with MN1-expressing retrovirus, had been transplanted. (C) Kaplan-Meier style survival curve of WT secondary recipient mice of sorted GFP (MLL-AF9)⁺ Lin^– BM cells from WT (red) or ANXA5-deficient (blue) primary donor mice with established MLL-AF9–induced AML (P = .01; log-rank test, n = 9-10). Mice were irradiated with 2 × 450 cGy, and 1.5 × 10⁴ GFP (MLL-AF9)⁺ Lin^– plus 2 × 10⁶ supporter BM cells had been transplanted. Median survival for WT recipients of Lin^– BM from WT mice was 63 days and for WT recipients of Lin^– BM from ANXA5-deficient mice was 54 days. (D) Number of colonies per plate derived from total BM (circles) or spleen (squares) cells from WT (red or ANXA5-deficient (blue) recipient mice with established MLL-AF9-induced AML plated in methylcellulose (P < .0001; 1-way analysis of variance [ANOVA]; Sidak test; n = 9).