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Tyrosine kinase oncogenes in normal hematopoiesis and hematological disease

Oncogene volume 21, pages 3314–3333 (2002)Cite this article

Abstract

Tyrosine kinase oncogenes are formed as a result of mutations that induce constitutive kinase activity. Many of these tyrosine kinase oncogenes that are derived from genes, such as c-Abl, c-Fes, Flt3, c-Fms, c-Kit and PDGFRβ, that are normally involved in the regulation of hematopoiesis or hematopoietic cell function. Despite differences in structure, normal function, and subcellular location, many of the tyrosine kinase oncogenes signal through the same pathways, and typically enhance proliferation and prolong viability. They represent excellent potential drug targets, and it is likely that additional mutations will be identified in other kinases, their immediate downstream targets, or in proteins regulating their function.

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Acknowledgements

B Scheijen provided the concept, design, collected the data, drafted the paper and gave final approval. JD Griffin drafted the paper and gave final approval. This work was supported by a fellowship of the Dutch Cancer Society (KWF) to B Scheijen.

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  1. Department of Adult Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, 02115, Massachusetts, MA, USA

    Blanca Scheijen & James D Griffin

  2. Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

    Blanca Scheijen & James D Griffin

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  1. Blanca Scheijen
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  2. James D Griffin
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Correspondence to James D Griffin.

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Scheijen, B., Griffin, J. Tyrosine kinase oncogenes in normal hematopoiesis and hematological disease. Oncogene 21, 3314–3333 (2002). https://doi.org/10.1038/sj.onc.1205317

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