Progenitor cell involvement is predictive of response to induction chemotherapy in paediatric acute myeloid leukaemia

Br J Haematol. 2003 Nov;123(3):431-5. doi: 10.1046/j.1365-2141.2003.04633.x.

Abstract

In acute myeloid leukaemia (AML), involvement of early progenitor cells may predict poor response to induction chemotherapy. We evaluated the involvement of early progenitor cells in two AML subtypes with a favourable prognosis [t(8;21) and t(15;17)], and a subtype with poor prognosis (monosomy 7). CD34+CD33- cells were isolated by fluorescence-activated cell sorting, grown in liquid medium followed by culture in semi-solid medium, and the colonies that were formed were analysed for the identifiable genetic markers. Two of 136 colonies from six t(8;21) AML patients expressed the AML1-ETO transcript, and all six patients achieved remission after induction. None of 192 colonies from five t(15;17) AML patients expressed the RARalpha-PML transcript and all achieved remission. In contrast, in three of 10 cases of monosomy 7 AML, colonies were positive for monosomy 7, and all three patients failed to enter remission. However, five of six evaluable patients with colonies negative for monosomy 7 entered remission. These data support the hypothesis that leukaemic involvement of early progenitor cells affects the response to induction chemotherapy.

Publication types

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

MeSH terms

  • Acute Disease
  • Child
  • Chromosome Aberrations*
  • Chromosomes, Human, Pair 15
  • Chromosomes, Human, Pair 17
  • Chromosomes, Human, Pair 21
  • Chromosomes, Human, Pair 7
  • Chromosomes, Human, Pair 8
  • Core Binding Factor Alpha 2 Subunit
  • Gene Rearrangement
  • Genetic Markers
  • Humans
  • In Situ Hybridization, Fluorescence
  • Leukemia, Myeloid / drug therapy*
  • Leukemia, Myeloid / genetics*
  • Monosomy
  • Neoplasm Proteins / genetics
  • Oncogene Proteins, Fusion / genetics
  • Prognosis
  • RUNX1 Translocation Partner 1 Protein
  • Remission Induction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stem Cells*
  • Transcription Factors / genetics
  • Translocation, Genetic

Substances

  • AML1-ETO fusion protein, human
  • Core Binding Factor Alpha 2 Subunit
  • Genetic Markers
  • Neoplasm Proteins
  • Oncogene Proteins, Fusion
  • RUNX1 Translocation Partner 1 Protein
  • Transcription Factors
  • promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein