SUMMARY
In 15–20% of children with acute myeloid leukaemia (AML), a mutation in the FMS-like tyrosine kinase 3 (FLT3) protein is present. This is usually an internal tandem duplication (FLT3-ITD), an activating mutation that ensures cell survival and proliferation. A FLT3-ITD mutation is associated with a lower chance of survival and is an indication for allogeneic stem cell transplantation (SCT) in children with AML. Since the risk of relapse after allogeneic SCT can be up to 40%, additional treatment after allogeneic SCT is also being investigated. In recent decades, several targeted therapies have been developed for patients with AML, including several generations of FLT3 inhibitors (tyrosine kinase inhibitors). The effect of these inhibitors has already been demonstrated in adult patients with AML; however, the role of FLT3 inhibitors in children with AML with an FLT3-ITD mutation is not yet fully understood. In this article, we discuss the role of FLT3 inhibitors after allogeneic stem cell transplantation for children with AML.
(BELG J HEMATOL 2023;14(8):331–5)
