AML1 amplification in a case of childhood acute lymphoblastic leukemia

Cancer Genet Cytogenet. 2002 Sep;137(2):142-5. doi: 10.1016/s0165-4608(02)00566-6.

Abstract

We report an 8-year-old girl with B-cell acute lymphoblastic leukemia (ALL). The blast cell karyotype at diagnosis included a marker chromosome revealed by fluorescence in situ hybridization to be a derivative of chromosome 21. A high level amplification of the AML1 gene was identified, but it disappeared upon complete remission. This rare but recurrent abnormality warrants research of B-cell ALL, especially when a marker chromosome is present in the blast cell karyotype.

Publication types

  • Case Reports

MeSH terms

  • Child
  • Chromosome Aberrations*
  • Chromosome Deletion
  • Chromosomes, Human, Pair 21 / genetics*
  • Core Binding Factor Alpha 2 Subunit
  • DNA-Binding Proteins / genetics*
  • Female
  • Gene Amplification*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Proto-Oncogene Proteins*
  • Transcription Factors / genetics*

Substances

  • Core Binding Factor Alpha 2 Subunit
  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • RUNX1 protein, human
  • Transcription Factors