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Growth factor independence and BCR/ABL transformation: promise and pitfalls of murine model systems and assays

Leukemia volume 13, pages 1200–1206 (1999)Cite this article

Abstract

The expression of the BCR-ABL fusion oncoprotein in primitive hematopoietic cells results in chronic myeloid leukemia. Over the past decade studies of several in vitro and in vivo cell systems revealed multiple signal transduction pathways activated by BCR-ABL. However, the precise function of BCR-ABL in the pathogenesis of CML is still unclear. The goal of this review is to synthesize data on intracellular signaling in the context of the diverse murine assay systems employed. We emphasize the importance of in vivo assays and assays using primary cells in understanding the biology of CML and the molecular mechanisms by which BCR-ABL exerts its effects.

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Authors and Affiliations

  1. Whitehead Institute for Biomedical Research, Cambridge, MA, USA

    S Ghaffari, GQ Daley & HF Lodish

  2. Division of Hematology-Oncology, Massachusetts General Hospital, Boston, MA, USA

    GQ Daley

  3. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA

    HF Lodish

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  1. S Ghaffari
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  2. GQ Daley
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  3. HF Lodish
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Ghaffari, S., Daley, G. & Lodish, H. Growth factor independence and BCR/ABL transformation: promise and pitfalls of murine model systems and assays. Leukemia 13, 1200–1206 (1999). https://doi.org/10.1038/sj.leu.2401467

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  • DOI: https://doi.org/10.1038/sj.leu.2401467

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