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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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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DOI: https://doi.org/10.1038/300765a0
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