Midostaurin in the treatment of patient with acute myeloid leukemia with FLT3-TKD mutation and NPM1 mutation

Abstract

Acute myeloid leukaemia (AML) is aggressive cancer with a diverse clinical course which mainly results from the heterogeneous and complex molecular landscape of the disease. For some genetic alterations, in particular mutations in the FSM-like tyrosine kinase 3 (FLT3) gene, the prognosis of patients with newly diagnosed AML depends on the coexistence of other genetic disorders. A thorough understanding of the interactions between mutations is key to improving risk stratification in newly diagnosed AML and personalizing therapy. The addition of midostaurin, an FLT3 tyrosine kinase inhibitor, to standard chemotherapy improved outcomes in the unfavourable prognostic group of AML patients. Here, we describe a therapeutic strategy in a patient with newly diagnosed AML with FLT3-tyrosine kinase domain (TKD) mutation and wild-type NPM1 who has received a standard remission induction and consolidation chemotherapy in combination with midostaurin, followed by maintenance therapy with an FLT3 inhibitor and haploidentical allogeneic hematopoietic stem cell transplantation.