Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation

Richard M. Stone; Sumithra J. Mandrekar; Ben L. Sanford; Kristina Laumann; Susan M. Geyer; Clara D. Bloomfield; Christian Thiede; Thomas W. Prior; Konstanze Döhner; Guido Marcucci; Francesco Lo‐Coco; Rebecca B. Klisovic; Andrew H. Wei; Jorge Sierra; Miguel Á. Sanz; Joseph Brandwein; Théo de Witte; Dietger Niederwieser; Frederick R. Appelbaum; Bruno C. Medeiros; Martin S. Tallman; Jürgen Krauter; Richard F. Schlenk; Arnold Ganser; Hubert Serve; Gerhard Ehninger; Sergio Amadori; Richard A. Larson; Hartmut Döhner

doi:10.1056/nejmoa1614359

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Abstract

The addition of the multitargeted kinase inhibitor midostaurin to standard chemotherapy significantly prolonged overall and event-free survival among patients with AML and a FLT3 mutation. (Funded by the National Cancer Institute and Novartis; ClinicalTrials.gov number, NCT00651261 .).

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Stone et al. (2017) studied this question.

synapsesocial.com/papers/69d9e808a1d151c65f68569c https://doi.org/10.1056/nejmoa1614359

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Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation

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Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation

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