Abstract
The transforming genes of acutely transforming retroviruses are derived from conserved cellular genes (c-onc genes) which are believed to be important in normal cell growth and differentiation1–4. Recent studies indicate that altered expression of c-onc genes, for example, by insertion of viral genomes5,6, gene amplification7,8 or chromosomal translocation9–12, can lead to development of malignant diseases in man and animals. c-myb and c-fes are homologues of the transforming genes of avian myeloblastosis virus and feline sarcoma virus (Gardner and Snyder–Theilen strains), respectively. c-myb is transcribed preferentially in immature haematopoietic cells13 and probably codes for a protein important in differentiation of these cells. The viral fes gene, like several other viral onc genes, encodes a tyrosine-specific protein kinase14. However, c-fes transcripts have not been detected in the types of human cells examined so far15,16. c-myb and c-fes have been assigned to human chromosomes 6 and 15, respectively17,18. Specific aberrations involving these chromosomes have been observed at high frequency in several human neoplasms19. We have now sub-localized c-myb to 6q22–24 and c-fes to 15q25–26 by in situ hybridization of the human c-onc probes to human mitotic chromosome preparations20,21. These chromosomal segments are indeed involved in nonrandom translocations in several human tumours. The results encourage further investigation into the role of onc genes in the pathogenesis of specific neoplasms.
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Harper, M., Franchini, G., Love, J. et al. Chromosomal sublocalization of human c-myb and c-fes cellular onc genes. Nature 304, 169–171 (1983). https://doi.org/10.1038/304169a0
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DOI: https://doi.org/10.1038/304169a0
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