[Molecular study of bone marrow chimerism and expression of EVI-1 gene as manifestations of minimal residual disease after bone marrow transplantation (BMT)]

Med Wieku Rozwoj. 1999 Jan-Mar;3(1):139-52.
[Article in Polish]

Abstract

Leukaemias are the most frequent tumour diseases in children. Bone marrow transplantation (BMT) is the most effective therapy for many patients with leukaemia. Highly polymorphic microsatellite markers provide useful genetic markers for detection of complete or mixed chimerism in patients after (BMT). Chimerism can be monitored successfully using several polymerase chain reaction (PCR) techniques and cytogenetic analysis, especially fluorescent in situ hybridization (FISH). It is still unclear whether individuals with mixed chimerism after bone marrow transplantation have an increased risk of developing leukaemic relapse or graft rejection. EVI-1 gene was mapped in human chromosome 3q26. It encodes zinc finger, DNA binding protein detected only in the nucleus. The EVI-1 function is unknown. It is not expressed in normal human haematopoietic cells, but is expressed in leukaemias especially with 3q26 abnormalities. Expression of the EVI-1 may play a significant role in pathogenesis of human leukaemias. Molecular study of chimerism and expression of EVI-1 gene may be useful for monitoring residual disease after bone marrow transplantation.

Publication types

  • Review

MeSH terms

  • Bone Marrow / pathology*
  • Bone Marrow Transplantation / adverse effects*
  • Child
  • Chromosome Mapping
  • Chromosomes, Human, Pair 3
  • DNA-Binding Proteins / genetics*
  • Genetic Markers
  • Humans
  • In Situ Hybridization, Fluorescence
  • Leukemia / genetics*
  • Leukemia / therapy*
  • MDS1 and EVI1 Complex Locus Protein
  • Neoplasm, Residual
  • Polymerase Chain Reaction
  • Proto-Oncogenes*
  • Recurrence
  • Transcription Factors*
  • Transplantation Chimera / genetics*

Substances

  • DNA-Binding Proteins
  • Genetic Markers
  • MDS1 and EVI1 Complex Locus Protein
  • MECOM protein, human
  • Transcription Factors