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Environmental carcinogenesis: an integrative model.

J E Trosko, C C Chang

    The Quarterly Review of Biology
    |June 1, 1978
    PubMed
    Summary
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    Environmental carcinogens alter genetic control of cell division and differentiation. This integrative theory combines mutation and epigenetic processes, suggesting carcinogens target regulatory genes controlling cell transformation.

    Area of Science:

    • Oncology
    • Genetics
    • Environmental Health

    Background:

    • Carcinogenesis theories include somatic mutation and epigenetic models.
    • Carcinogens encompass physical, chemical, and viral agents acting as mutagens or gene modulators.
    • Existing theories offer partial explanations for cancer development.

    Purpose of the Study:

    • To propose an integrative theory of environmental carcinogenesis.
    • To reconcile somatic mutation and epigenetic theories of cancer.
    • To present a unifying framework for understanding cancer initiation.

    Main Methods:

    • Review and integration of existing carcinogenesis theories (e.g., two-stage, Comings').
    • Analysis of evidence supporting both mutational and epigenetic mechanisms.

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  • Postulation of a common mechanism involving DNA damage repair.

    • Main Results:

    • Evidence supports a dual role for mutations and epigenetic alterations in carcinogenesis.
    • Carcinogens are proposed to affect regulatory genes controlling cell division and differentiation.
    • A common mechanism of somatic mutagenesis via error-prone DNA repair is hypothesized.

    Conclusions:

    • An integrative theory provides a comprehensive view of environmental carcinogenesis.
    • Carcinogens likely target regulatory genes, impacting cell division and differentiation pathways.
    • The proposed mechanism links cancer, teratogenesis, atherosclerosis, and aging.