Treatment of Acute Myeloid Leukemia with the FLT3 Gene Mutation

Curr Oncol Rep. 2017 Mar;19(3):21. doi: 10.1007/s11912-017-0573-x.

Abstract

In acute myeloid leukemia (AML), mutations of the Fms-like tyrosine kinase 3 receptor (FLT3) and its overexpression are related with hyperleukocytosis, higher risk of relapse, and decrease of both disease-free survival and overall survival. It has been suggested that this phenomenon confers proliferative and survival advantages to the malignant blast cells. As a consequence, it is an attractive therapeutic target. As the best treatment strategy for mutated FLT3 AML remains to be defined, the addition of FLT3 inhibitor drugs to chemotherapy or to the bone marrow transplant approach has become a growing strategy. With encouraging results, this combination seems to be an attractive option. Relevant data regarding the current treatment trends on mutated FLT3 AML is reviewed here.

Keywords: Acute myeloid leukemia treatment; FLT3 inhibitor drugs; FLT3 mutations.

Publication types

  • Review

MeSH terms

  • Cell Proliferation / drug effects
  • Disease-Free Survival
  • Humans
  • Leukemia, Myeloid, Acute / drug therapy*
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / pathology
  • Molecular Targeted Therapy*
  • Mutation
  • Protein Kinase Inhibitors / therapeutic use
  • fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • fms-Like Tyrosine Kinase 3 / genetics*

Substances

  • Protein Kinase Inhibitors
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3