Chapter 20. The Role of RARα and Its Fusion Partners in Acute Promyelocytic Leukemia

  1. Katya Ravid2,
  2. Jonathan D. Licht3
  1. Ari Melnick1,
  2. Jonathan D. Licht3

Published Online: 19 MAR 2002

DOI: 10.1002/0471223883.ch20

Book Title

Transcription Factors: Normal and Malignant Development of Blood Cells

Transcription Factors: Normal and Malignant Development of Blood Cells

Additional Information

How to Cite

Melnick, A. and Licht, J. D. (2002) The Role of RARα and Its Fusion Partners in Acute Promyelocytic Leukemia, 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.ch20

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. 1

    Mount Sinai School of Medicine, Ruttenberg Cancer Center, Departments of Medicine and Molecular Biology, Box 1130, One Gustave Lower Levy Place, New York, NY 10029

  2. 3

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

Publication History

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

ISBN Information

Print ISBN: 9780471350545

Online ISBN: 9780471223887

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Keywords:

  • retinoic acid receptor alpha (RARα);
  • transcriptional function;
  • myeloid differentiation;
  • target genes;
  • acute promyelocytic leukemia (APL);
  • PML-RARα;
  • promyelocytic leukemia zinc finger (PLZF);
  • PLZF-RARα;
  • RARα-PLZF;
  • nucleophosmin;
  • NPM-RARα;
  • NuMA-RARα;
  • STAT5b-RARα

Summary

Acute promyelocytic leukemia (APL) is now associated with five different gene rearrangements, fusing retinoic acid receptor alpha (RARα) to the promyelocytic leukemia (PML) gene, promyelocytic leukemia zinc finger (PLZF), nucleophosmin (NPM), nuclear matrix-associated (NuMA) and STAT5b genes, leading to the formation of reciprocal fusion proteins (N-RARα and RARα-N). Disruption of both RAR and the partner gene function may both play roles in the pathogenesis of the disease.

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