Abstract
RECENT studies of factors modifying the response of mammalian tissues to radiation have led to results which cannot be interpreted on existing theories, and a more comprehensive hypothesis on the nature of radiation reactions in multicellular organisms seems necessary. Previous studies on the C3H mouse mammary carcinoma had shown that its radiosensitivity apparently depends on an auto-immunizing mechanism or similar manifestation of host resistance, and is consequently determined largely by the degree of genetic and antigenic diversification between host and tumour. This interpretation, however, is not sufficient to explain more recent results on the induced radiosensitization of unmodified isogenic tumours by inoculation of the host with a second, suitably attenuated, inoculum. For example, irradiated isogenic tissues, including tumour isografts given a dose sufficient to prevent their ‘taking’, will, when inoculated into a mouse already bearing a growing tumour graft, render the established tumour materially more radiosensitive1.
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COHEN, L., COHEN, A. Radiosensitivity as a Function of Antigenic Equivocation. Nature 183, 692–693 (1959). https://doi.org/10.1038/183692a0
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DOI: https://doi.org/10.1038/183692a0
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