Fig. 3
From: Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms
RAS pathway mutations contribute to crenolanib resistance and disease relapse. a The graph depicts variant allele frequencies (VAFs) of FLT3-ITD/TKD and RAS pathway mutations during crenolanib treatment. b Graph depicts higher mean ± SEM of cell viabilities of crenolanib-treated PTPN11 A72D/ FLT3 D835Y Ba/F3 cells in comparison to PTPN11 WT/ FLT3 D835Y co-expressing Ba/F3 cells and FLT3 D835Y-alone expressing Ba/F3 cells determined by MTS assay. c Graph depicts mean ± SEM of crenolanib half-maximal inhibitory concentration (IC50) in (b). Data shown are from five biological replicates. Statistical significance was assessed using one-way analysis of variance (ANOVA) together with Dunn’s multiple comparisons tests and expressed as: *p < 0.05
