The majority of myeloid-antigen-positive (My+) childhood B-cell precursor acute lymphoblastic leukaemias express TEL-AML1 fusion transcripts

Br J Haematol. 1997 Oct;99(1):101-6. doi: 10.1046/j.1365-2141.1997.3603174.x.

Abstract

The t(12:21) translocation fuses the TEL and AML1 genes and has been found in up to 28% of paediatric B-cell precursor acute lymphoblastic leukaemias (BCP-ALL). The AML1 gene is a transcription factor which regulates expression of several myeloid differentiation associated genes. A molecular analysis of TEL-AML1, E2A-PBX1, MLL-AF4, BCR-ABL expression and an immunophenotypic study of CD13/CD33 myeloid antigen expression have been performed prospectively on tumour cells from 96 paediatric BCP-ALL patients. Percentages of CD13 or CD33 expressing leukaemic cells were found to be higher in TEL-AML1 positive cases (n = 22) than in TEL-AML1 negative (n = 74) cases (P<0.001). In 22/96 cases (23%) >10% of neoplastic cells were found to express at least one of the two markers. In 14 of these cases (63%), TEL-AML1 expression was detected, whereas t(4;11), t(11;19) and t(9;22) translocations were found by molecular methods in only three cases (14%). In four cases (18%) no molecular marker was found. These data show that TEL-AML1 expression is significantly associated with myeloid antigen expression by leukaemic cells and suggests that the prognostic significance of myeloid antigen expression in paediatric ALLs should be re-evaluated in the light of molecular cytogenetic markers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Differentiation, Myelomonocytic / metabolism*
  • Blotting, Southern
  • Child
  • Child, Preschool
  • Chromosomes, Human, Pair 12 / genetics
  • Chromosomes, Human, Pair 21 / genetics
  • Fusion Proteins, bcr-abl / metabolism
  • Humans
  • Immunophenotyping
  • Oncogene Proteins, Fusion / metabolism*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
  • Transcription Factors / metabolism*
  • Translocation, Genetic / genetics

Substances

  • Antigens, Differentiation, Myelomonocytic
  • Oncogene Proteins, Fusion
  • Transcription Factors
  • Fusion Proteins, bcr-abl