The Future of Targeting FLT3 Activation in AML

Mark B. Leick, Mark J Levis

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)1-15
Number of pages15
JournalCurrent Hematologic Malignancy Reports
DOIs
StateAccepted/In press - Apr 18 2017

Keywords

  • Acute myeloid leukemia (AML)
  • FLT3
  • Tyrosine-kinase inhibitor (TKI)

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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