Fig. 2
From: Partial p53 reactivation is sufficient to induce cancer regression
In vitro response of p53-deficient AML to E177R activation. a Flow cytometry of BrdU and propidium iodide (PI)-stained LSL-E177R; CreERT2 (LSL) AML cells 72 h after indicated treatment. KO; CreERT2 (KO) AML cells are shown as controls. The percentage of cells in S phase is indicated. b Senescence-associated β-galactosidase staining of LSL and KO AML cells 1 week after indicated treatment. c Flow cytometry of LSL AML cells stained for differentiation markers (Lin, CD11b, Gr-1) 48 h after indicated treatment. d Flow cytometry of LSL AML cells stained for the apoptosis markers annexin V and cleaved caspase-3 (CC3) 48 h after indicated treatment. e Clonogenic growth assay of AML cells with indicated genotype and treatment grown in MethoCult medium for 1 week. In all experiments, cells were treated with 1 μM 4OHT or solvent (ethanol) as the mock control. All quantification bar graphs show mean ± SD; datapoints represent biological replicates; reported are P-values of a two-tailed unpaired t-test