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onc gene amplification in promyelocytic leukaemia cell line HL-60 and primary leukaemic cells of the same patient

Nature volume 299, pages 61–63 (1982)Cite this article

Abstract

Cellular onc genes are a group of evolutionarily conserved sequences which are homologous to the transforming genes (v-onc) of oncogenic retroviruses1. Their function in normal cells is not yet known, but the sequence homology between viral and cellular onc genes is consistent with the idea that neoplastic transformation may, in some cases, be due to increased levels of cellular onc gene expression. The cellular homologue, c-myc, of the transforming gene of avian myelocytomatosis virus (MC29)1,2 is involved in the pathogenesis of chicken B-cell lymphomas induced by the non-acute leukosis virus (RAV-2)3–6, and in these tumours, c-myc expression is enhanced by the nearby integration of the RAV-2 terminal repeat region3–6. Transcripts from the c-myc gene are detectable in a variety of human cells7,8, and increased levels of myc mRNA have been occasionally detected in some neoplastic tissues7,8. The highest levels have been detected in the cell line HL-60 (ref. 8) derived from neoplastic cells from a patient with acute promyelocytic leukaemia (APL)9. We have now investigated whether any structural alteration at the genomic level could account for the increased expression of c-myc in HL-60 and report here that the c-myc gene is stably amplified in HL-60 DNA. Amplification was also detected in primary uncultured leukaemic cells from the same individual, suggesting that the c-myc amplification may have been involved in the leukaemic transformation in this case.

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Authors and Affiliations

  1. Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, 20205, USA

    Riccardo Dalla Favera, Flossie Wong-Staal & Robert C. Gallo

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  1. Riccardo Dalla Favera
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  2. Flossie Wong-Staal
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  3. Robert C. Gallo
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Favera, R., Wong-Staal, F. & Gallo, R. onc gene amplification in promyelocytic leukaemia cell line HL-60 and primary leukaemic cells of the same patient. Nature 299, 61–63 (1982). https://doi.org/10.1038/299061a0

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