Abstract
The localization of cellular oncogenes near the break points of tumour-specific chromosomal aberrations suggests an involvement of these genes in the generation of neoplasms. Recently, we demonstrated the translocation of the human cellular homologue (c-ab1) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) from chromosome 9 to the Philadelphia chromosome (Ph1) in chronic myelocytic leukaemia (CML). In an attempt to investigate the significance of this translocation in the pathogenesis of CML, we have now studied two CML patients with complex translocations, t(9; 11; 22) and t(1; 9; 22), and two CML Ph1-negative patients with apparently normal karyotypes. In addition to using blot hybridization with human c-ab1 probes and DNA from rodent: CML cell hybrids as before, we have used in situ hybridization of these probes directly to metaphase chromosomes of CML patients. These studies show that the c-ab1 gene is translocated in Ph1-positive but not in Ph1-negative CML patients. CML without the Ph1 chromosome seems to be a distinct entity with a different origin, and this view is supported by clinical observations including correlations which reveal a poorer prognosis.
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