Chapter 24. TEL/ETV6 Gene Rearrangements in Human Leukemias

  1. Katya Ravid2,
  2. Jonathan D. Licht3
  1. Ema Anastasiadou,
  2. Michael H. Tomasson,
  3. David W. Sternberg,
  4. Todd R. Golub,
  5. D. Gary Gilliland

Published Online: 19 MAR 2002

DOI: 10.1002/0471223883.ch24

Transcription Factors: Normal and Malignant Development of Blood Cells

Transcription Factors: Normal and Malignant Development of Blood Cells

How to Cite

Anastasiadou, E., Tomasson, M. H., Sternberg, D. W., Golub, T. R. and Gilliland, D. G. (2002) TEL/ETV6 Gene Rearrangements in Human Leukemias, in Transcription Factors: Normal and Malignant Development of Blood Cells (eds K. Ravid and J. D. Licht), John Wiley & Sons, Inc., New York, USA. doi: 10.1002/0471223883.ch24

Editor Information

  1. 2

    Department of Biochemistry, Boston University School of Medicine, Boston, MA

  2. 3

    Derald H. Ruttenberg Cancer Center and Department of Medicine, Mount Sinai School of Medicine, New York, NY

Author Information

  1. Harvard Institutes of Medicine, Room 421, 4 Blackfan Circle, Boston, MA 02115

Publication History

  1. Published Online: 19 MAR 2002
  2. Published Print: 15 DEC 2000

ISBN Information

Print ISBN: 9780471350545

Online ISBN: 9780471223887

SEARCH

Keywords:

  • TEL/ETV6 gene rearrangements;
  • TEL gene product;
  • hematopoiesis;
  • hematologic malignancies;
  • human cancers;
  • human leukemia;
  • TEL/tyrosine kinase functions;
  • TEL/AML1 fusion;
  • pediatric acute lymphoblastic leukemia (ALL);
  • core-binding factor complex

Summary

Although many questions remain about the molecular mechanisms of transformation, clinically useful insights have been gained from analysis of hematologic malignancies that harbor TEL gene rearrangements. Analysis of the TEL-tyrosine kinase fusions has demonstrated that at a minimum the kinase is an appropriate and tenable target for therapeutic intervention, and that some downstream effectors of transformation such as Stat family members may also be potential targets for drug development.