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

Nature. 1982 Dec 23;300(5894):765-7. doi: 10.1038/300765a0.


The transforming genes of oncogenic retroviruses are homologous to a group of evolutionary conserved cellular onc genes. The human cellular homologue (c-abl) of the transforming sequence of Abelson murine leukaemia virus (A-MuL V) was recently shown 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 chromosomes and suggests a role for the c-abl gene in the generation of CML.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Chromosomes, Human, 21-22 and Y*
  • Chromosomes, Human, 6-12 and X*
  • DNA, Neoplasm / genetics
  • Gene Expression Regulation
  • Humans
  • Leukemia, Myeloid / genetics*
  • Oncogenes*
  • Translocation, Genetic


  • DNA, Neoplasm