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Cancer genes: rare recombinants instead of activated oncogenes (a review)

P H Duesberg

    Proceedings of the National Academy of Sciences of the United States of America
    |April 1, 1987
    PubMed

    Insights

    Viral oncogenes are new recombinants, not transduced cellular cancer genes. Proto-oncogenes are not latent cancer genes; rare genetic alterations likely generate cancer genes, supported by tumor cell chromosomal abnormalities.

    Area of Science:

    • Molecular Biology
    • Oncology
    • Genetics

    Background:

    • Retroviral oncogenes (onc) are derived from cellular proto-oncogenes.
    • A popular hypothesis suggests proto-oncogenes are latent cancer genes activated in virus-negative tumors.
    • This hypothesis implies direct access to cellular cancer genes.

    Purpose of the Study:

    • To investigate the origin and function of viral oncogenes and proto-oncogenes.
    • To evaluate the hypothesis that proto-oncogenes act as latent cellular oncogenes.
    • To propose an alternative mechanism for cancer gene generation.

    Main Methods:

    • Structural comparison of viral oncogenes, retroviral genes, and proto-oncogenes.
    • Analysis of proto-oncogene expression in normal cells.
    • Examination of experimental data on cell transformation and tumor formation.

    Main Results:

    • Viral oncogenes are novel recombinants of truncated viral and proto-oncogenes, not direct transductions.
    • Proto-oncogenes are commonly expressed in normal cells.
    • No evidence supports proto-oncogenes as latent cancer genes inducing tumors; experimental predictions remain unconfirmed.

    Conclusions:

    • The hypothesis of proto-oncogenes as latent cellular oncogenes is an overinterpretation.
    • Cancer genes likely arise from rare germ-line alterations, truncations, and illegitimate recombinations.
    • Clonal chromosomal abnormalities in tumors provide evidence for rearrangements generating cancer genes.

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