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. 2020 Mar 5;12(4):e10895. doi: 10.15252/emmm.201910895

Figure 8. Schematic diagram depicting the molecular mechanism of FST upregulation in FLT3/ITD‐transgenic zebrafish, knock‐in mice, and human AML .

Figure 8

Left panel. Transient overexpression of human FLT3/ITD mutation resulted in axis duplication and dorsalization abnormalities in zebrafish accompanied by upregulation of embryonic morphogen Fst. Upregulation of FST was consistently found in FLT3/ITD‐transgenic zebrafish, Flt3/ITD knock‐in mice, FLT3/ITD‐mutated AML cell lines, and primary AML samples in vitro and in vivo. Right panel. A novel FLT3/ITD‐p90RSK‐CREB‐FST signaling cascade was demonstrated in human AML. FST is a promising biomarker and therapeutic target for human FLT3/ITD+ AML.