FLT3-mutated acute myeloid leukaemia: a new opportunity
Mené dans 26 pays sur 539 patients atteints d'une leucémie myéloïde aiguë présentant des duplications internes en tandem au niveau du gène FLT3 et récemment diagnostiquée (âge : 18-75 ans), cet essai randomisé de phase III évalue l'efficacité, du point de vue de la survie globale, et la toxicité de l'ajout du quizartinib (un inhibiteur sélectif anti-FLT3 de type 2 dispensé par voie orale) à un traitement d'induction ou de consolidation par chimiothérapie
Acute myeloid leukaemia (AML) is a heterogeneous, aggressive malignancy of immature myeloid progenitors with poor survival. 1 Approximately 30% of patients with newly diagnosed AML have fms-related tyrosine kinase 3 (FLT3) mutations, most of which are internal tandem duplications (ITD). 2 Historically, FLT3-positive AML, particularly FLT3-ITD-positive AML, has been associated with relapse and poor survival. 1 , 2 Since 2017, routine referral for allogeneic stem-cell transplant (ASCT) and regulatory approval of the multikinase inhibitor midostaurin in combination with standard chemotherapy (on the basis of data from the RATIFY study) 2 for both FLT3-ITD-positive and FLT3-tyrosine-kinase-domain-positive newly diagnosed AML have improved outcomes. 2 , 3 Midostaurin plus chemotherapy improves median overall survival (74 months vs 26 months) and event-free survival (8 months vs 3 months), and is now the standard of care for chemotherapy-eligible patients with FLT3-positive AML
The Lancet , commentaire, 2022