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Carcinogenesis in relation to the stem-cell-mutation hypothesis.

S Kondo

    Differentiation; Research in Biological Diversity
    |January 1, 1983
    PubMed
    Summary
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    Vertebrates are resistant to carcinogens during early development. Tumor development is initiated by stem cell mutations during organogenesis, supported by heritable tumor induction studies.

    Area of Science:

    • Developmental Biology
    • Cancer Research
    • Molecular Biology

    Background:

    • Early developmental stages in vertebrates, particularly before organogenesis, exhibit resistance to carcinogen-induced tumors.
    • Studies on chemical carcinogenesis in mice provide insights into the molecular mechanisms underlying tumor formation.
    • Heritable tumors in mice and Drosophila, induced by germ cell exposure to radiation and chemicals, offer evidence for mutations causing cancer.

    Purpose of the Study:

    • To explore the hypothesis that organ carcinogenesis is initiated by stem cell mutations during organogenesis.
    • To discuss the relationship between tumorigenesis and teratogenesis.
    • To examine the susceptibility of growing or regenerating organs to carcinogens and the latent period of induced neoplasms in the context of the stem-cell-mutation hypothesis.

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    Main Methods:

    • Review of existing reports on tumor induction by carcinogens in various species (fish, mice, rats, humans).
    • Analysis of molecular biology data related to chemical carcinogenesis in mice.
    • Examination of evidence for heritable tumor induction and the nature of tumor genes.

    Main Results:

    • Vertebrates are resistant to carcinogen-induced tumors before organogenesis.
    • Carcinogenesis of an organ is hypothesized to be initiated by mutations in stem cells formed during organogenesis.
    • Tumor genes, predisposing carriers to tumors, are suggested to be partly regulatory mutations.

    Conclusions:

    • The stem-cell-mutation hypothesis provides a framework for understanding tumor development.
    • The interrelation of tumorigenesis and teratogenesis, organ susceptibility, and latent periods are consistent with stem cell mutation initiation.