International Journal of Hematology

, Volume 76, Issue 1, pp 35–43

Bcr-Abl is a “Molecular Switch” for the Decision for Growth and Differentiation in Hematopoietic Stem Cells

Review Article

DOI: 10.1007/BF02982716

Cite this article as:
Era, T. Int J Hematol (2002) 76: 35. doi:10.1007/BF02982716


Chronic myeloid leukemia (CML) is a clonal disorder originating in the pluripotent hematopoietic stem cell (HSC), the hallmark of which is the constitutively activated p210-type of Bcr-Abl tyrosine kinase protein. Studies in recent years have helped us to understand the molecular processes involved in the initiation and progression of CML. Although a great amount of knowledge has been accumulated, the effect of Bcr-Abl on the HSC is still unclear. We have developed an in vitro system that mirrors the chronic phase of CML with a combination of in vitro embryonic stem cell differentiation and tetracycline-inducible Bcr-Abl expression. Enforced Bcr-Abl expression was sufficient to increase the number of both multilineage progenitors and myeloid progenitors.The current system is powerful for analyzing the genetic changes in hematopoietic development. This review focuses on how Bcr-Abl affects HSCs and how Bcr-Abl expression alters the properties of HSCs.

Key words

Chronic myeloid leukemia Bcr-Abl In vitro ES cell differentiation system Tetracycline regulatory system Hematopoietic stem cell 

Copyright information

© The Japanese Society of Hematology 2002

Authors and Affiliations

  1. 1.Stem Cell Biology GroupRIKEN Center for Developmental BiologyKobe City, HyogoJapan

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