Fig. 1

Development of AML in FCN mice. a WB of blood samples after erythrocyte lysis before and after induction of NFATc1 expression with tamoxifen treatment of mice. b Kaplan Meier survival curve of WT (n = 12), CN (n = 43), F (n = 33), FCN (n = 28); p < 0.0001. c, d Spleen weight (mean ± SD, n = 10 to 18 per group) (c), examples of spleens at 4 months (d). e, f Peripheral white blood counts (e) and platelet counts (f) over months 1 to 3 (mean ± SEM, n = 4 to 10 per group); p < 0.001. g Peripheral blood smears in F and FCN mice: left shifted hematopoiesis and increased white blood counts in FCN compared to F animals. Scale bars, 50 μm. h Bone marrow smears and IHC of bone marrow, histology of spleen and liver of WT, CN, F, and FCN mice. Black arrows highlight brownish cytoplasmic NFATC1 with sparing of blueish nuclear staining. Red arrows indicate nuclear NFATC1. Massive leukemic infiltrates cause a loss of normal tissue structure of spleen and liver in FCN. There are only minor tissue infiltrations in F and normal tissue structure in the CN animals. Bone marrow smears and the bone marrow histology of the FCN mice show increased cellularity, monomorphic infiltrates, as well as restricted erythro- and thrombopoiesis. FCN bone marrow shows stronger colorization and nuclear NFATC1 staining versus cytoplasmic staining patterns in the other genotypes. Scale bars, 100 μm. A Log-rank test (***p < 0.0001) or 1-way ANOVA (***p < 0.001) was used for p values