Fig. 1: Identification of potential key factors for FLT3i resistance. | Nature Communications

Fig. 1: Identification of potential key factors for FLT3i resistance.

From: Targeting C/EBPα overcomes primary resistance and improves the efficacy of FLT3 inhibitors in acute myeloid leukaemia

Fig. 1: Identification of potential key factors for FLT3i resistance.The alternative text for this image may have been generated using AI.

A Simplified schematic integrating patient clinical, WES, RNA-seq and FLT3i in vitro screening data to identify biomarkers predicting FLT3i response. B AUCs of four FLT3i from primary AML samples in Vizome (gilteritinib, n = 30; quizartinib, n = 56; midostaurin, n = 60; crenolanib, n = 54) were compared with blasts (%) in bone marrow (BM) and peripheral blood (PB). Significance was determined by the Spearman method. P < 0.05 represented significance, and R < 0 represented a negative correlation. The Y-axis indicates the AUC of the patient sample to FLT3i. C The AUCs of four FLT3i in AML common somatic mutation groups. AUCs in per group are presented as mean ± SEM. Significance was determined by the two-sided Wilcoxon rank sum test. Common differentially expressed reactome signalling pathways (D) and transcription factors (TFs) determined by GSEA (E). GSEA enrichment profiles (included p-value and enrichment score) of C/EBPα target genes in four FLT3i-resistant FLT3-ITD AML patients (F). Exact p values in Source Data file. Data for all graphs in Source Data file.

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