Activating FLT3 mutations in CD117/KIT(+) T-cell acute lymphoblastic leukemias

Blood. 2004 Jul 15;104(2):558-60. doi: 10.1182/blood-2004-01-0168. Epub 2004 Mar 25.


Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL (T-ALL) cases that coexpress CD117/KIT and cytoplasmic CD3 (CD117/KIT(+) ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/KIT(+) cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of patients with T-ALL.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Leukemic
  • Humans
  • Molecular Sequence Data
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-kit / genetics*
  • Proto-Oncogene Proteins c-kit / metabolism*
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • fms-Like Tyrosine Kinase 3


  • Proto-Oncogene Proteins
  • FLT3 protein, human
  • Proto-Oncogene Proteins c-kit
  • Receptor Protein-Tyrosine Kinases
  • fms-Like Tyrosine Kinase 3