International Journal of Hematology

, 73:278

Mechanisms of Transformation by the BCR/ABL Oncogene

Progress in hematology

DOI: 10.1007/BF02981952

Cite this article as:
Sattler, M. & Griffin, J.D. Int J Hematol (2001) 73: 278. doi:10.1007/BF02981952

Abstract

The Philadelphia chromosome generates a chimeric oncogene in which the BCR and c-ABL genes are fused. The product of this oncogene, BCR/ABL, has elevated ABL tyrosine kinase activity, relocates to the cytoskeleton, and phosphorylates mul-tiple cellular substrates. BCR/ABL transforms hematopoietic cells and exerts a wide variety of biological effects, including reduction in growth factor dependence, enhanced viability, and altered adhesion of chronic myelocytic leukemia (CML) cells. Elevated tyrosine kinase activity of BCR/ABL is critical for activating downstream signal transduction and for all aspects of transformation.This review will describe mechanisms of transformation by the BCR/ABL oncogene and opportunities for clin-ical intervention with specific signal transduction inhibitors such as STI-571 in CML.

Key words

BCR/ABLSignal transductionChronic myelogenous leukemia

Copyright information

© The Japanese Society of Hematology 2001

Authors and Affiliations

  1. 1.Department of Adult Oncology, Dana-Farber Cancer Institute, Department of MedicineBrigham and Women’s Hospital and Harvard Medical SchoolBostonUSA
  2. 2.Department of Adult Oncology, Dana-Farber Cancer Institute, Department of MedicineBrigham and Women’s Hospital and Harvard Medical SchoolBostonUSA