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Susceptibility determinants for mouse epidermal carcinogenesis

J E Strickland, H Hennings, A M Jetten

    IARC Scientific Publications
    |January 1, 1982
    PubMed
    Summary
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    SENCAR mice show higher susceptibility to skin cancer than BALB/c mice, primarily due to differences in the target skin tissue, not DNA repair or growth factor receptors.

    Area of Science:

    • Carcinogenesis
    • Dermatology
    • Genetics

    Background:

    • SENCAR mice are significantly more susceptible to two-stage skin carcinogenesis compared to BALB/c mice.
    • Understanding the basis of this differential susceptibility is crucial for skin cancer research.

    Purpose of the Study:

    • To investigate the underlying mechanisms responsible for the higher susceptibility of SENCAR mice to skin carcinogenesis.
    • To determine if differences in target tissue, DNA repair, or growth factor signaling contribute to this sensitivity.

    Main Methods:

    • Skin grafting experiments comparing SENCAR and BALB/c skin on nude mice.
    • Assessment of DNA repair capacity using host cell reactivation of UV-irradiated herpes simplex virus.
    • Analysis of epidermal growth factor (EGF) binding and responses to retinoic acid and phorbol esters.

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  • Evaluation of spontaneous xenotropic C RNA virus expression and differentiation-resistant foci in vitro.

    • Main Results:

    • SENCAR skin grafts on nude mice developed papillomas frequently, while BALB/c skin grafts did not, indicating target tissue determination.
    • DNA repair capacities were similar between SENCAR and BALB/c epidermal cells.
    • SENCAR cells showed greater epidermal growth factor binding, but responses to other factors were similar.
    • BALB/c cells exhibited more spontaneous endogenous virus expression, whereas SENCAR cells had more differentiation-resistant foci.

    Conclusions:

    • Skin carcinogenesis susceptibility in SENCAR mice is primarily determined by the target epidermal tissue.
    • Differences in DNA excision repair, endogenous virus complement, or epidermal growth factor receptors do not appear to be the primary drivers of this susceptibility.