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The Future of Targeting FLT3 Activation in AML

  • Acute Myeloid Leukemias (H Erba, Section Editor)
  • Published:
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Abstract

Internal tandem duplications (ITD) and tyrosine-kinase domain (TKD) mutations of the FMS-like tyrosine-kinase 3 (FLT3) can be found in up to one third of patients with acute myeloid leukemia (AML) and confer a poor prognosis. First discovered 20 years ago, these mutations were identified as viable therapeutic targets, and FLT3 tyrosine-kinase inhibitors (TKIs) have been in development for the last decade with steadily increasing potency. However, FLT3-mutated AML often acquires resistance to the growing armamentarium of FLT3 inhibitors through a variety of mechanisms. In this review, we discuss the distinct clinical phenotype of FLT3-mutated AML, historically and currently available therapeutics, mechanisms of resistance, ongoing trials, and future outlook at treatment strategies.

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Authors and Affiliations

  1. Department of Medicine, Johns Hopkins University, 600 North Wolfe Street, Harvey 805, Baltimore, MD, 21287, USA

    Mark B. Leick

  2. Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, 1650 Orleans Street, Cancer Research Building 1, Room 2M44, Baltimore, MD, 21287, USA

    Mark J. Levis

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Mark B. Leick declares no potential conflicts of interest. Mark J. Levis reports grants from Novartis and Astellas and consultancies for Novartis and Daiichi-Sankyo.

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This article is part of the Topical Collection on Acute Myeloid Leukemias

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Leick, M.B., Levis, M.J. The Future of Targeting FLT3 Activation in AML. Curr Hematol Malig Rep 12, 153–167 (2017). https://doi.org/10.1007/s11899-017-0381-2

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