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. 2017 Nov 1;8(62):105440–105457. doi: 10.18632/oncotarget.22241

Figure 8. A schematic of the proposed mechanism of FLT3-ITD-driven NOX4D-generated H2O2 in AML.

Figure 8

GSK3β, ERK1/2, PI3K/AKT and STAT5 pro-survival pathways are located downstream of FLT3-ITD. Activation of AKT and STAT5 signalling by the FLT3-ITD oncogene results in the activation and production of DNA damaging NOX4D-generated H2O2 at the nuclear membrane.