TRANSLOCATION OF C-ABL ONCOGENE CORRELATES WITH THE PRESENCE OF A PHILADELPHIA-CHROMOSOME IN CHRONIC MYELOCYTIC-LEUKEMIA
TRANSLOCATION OF C-ABL ONCOGENE CORRELATES WITH THE PRESENCE OF A PHILADELPHIA-CHROMOSOME IN CHRONIC MYELOCYTIC-LEUKEMIA
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DOI:
10.1038/306277a0
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发表时间:
1983-01-01
期刊:
影响因子:
64.8
通讯作者:
GROFFEN, J
中科院分区:
文献类型:
--
作者:
BARTRAM, CR;DEKLEIN, A;GROFFEN, J
The localization of cellular oncogenes near the break points of tumour-specific chromosomal aberrations suggests an involvement of these genes in the generation of neoplasms1,2. Recently, we demonstrated3the translocation of the human cellular homologue (c-abl) 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 translations, 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-ablprobes and DNA from Rodent: CML cell hybrids as before, we have usedin situhybridization of these probes directly to metaphase chromosomes of CML patients. These studies show that the c-ablgene is translocated in Ph1-positive but not in Ph1-negative CML patients. CML without the Ph1chromosome seems to be a distince entity with a different origin, and this view is supported by clinical observations including correlations which reveal a poorer prognosis4,5.