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A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia

Nature volume 300, pages 765–767 (1982)Cite this article

Abstract

The transforming genes of oncogenic retroviruses are homologous to a group of evolutionary conserved cellular onc genes1. The human cellular homologue (c-abl) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) was recently shown2 to be located on chromosome 9. The long arm of this chromosome is involved in a specific translocation with chromosome 22, the Philadelphia translocation (Ph1), t(9;22) (q34, q11), which occurs in patients with chronic myelocytic leukaemia (CML)3–5. Here we investigate whether the c-abl gene is included in this translocation. Using c-abl and v-abl hybridization probes on blots of somatic cell hybrids, positive hybridization is found when the 22q−(the Philadelphia chromosome), and not the 9q+ derivative of the translocation, is present in the cell hybrids. From this we conclude that in CML, c-abl sequences are translocated from chromosome 9 to chromosome 22q−. This finding is a direct demonstration of a reciprocal exchange between the two chromosomes6 and suggests a role for the c-abl gene in the generation of CML.

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Authors and Affiliations

  1. Department of Cell Biology and Genetics, Erasmus University, PO Box 1738, 3000 DR, Rotterdam, The Netherlands

    Annelies de Klein, Ad Geurts van Kessel, Gerard Grosveld, Claus R. Bartram, Anne Hagemeijer & Dirk Bootsma

  2. Imperial Cancer Research Fund, Lincoln's Inn Fields, London, WC2A 3PX, UK

    Nigel K. Spurr

  3. Laboratory of Viral Carcinogenesis, National Cancer Institute-FCRF, Frederick, Maryland, 21701, USA

    Nora Heisterkamp, John Groffen & John R. Stephenson

Authors
  1. Annelies de Klein
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  2. Ad Geurts van Kessel
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  3. Gerard Grosveld
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  4. Claus R. Bartram
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  5. Anne Hagemeijer
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  10. John R. Stephenson
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Klein, A., Kessel, A., Grosveld, G. et al. A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia. Nature 300, 765–767 (1982). https://doi.org/10.1038/300765a0

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