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The studies of Berenblum, Shubik, and others1 have shown that a single small dose of DMBA topically applied to mouse skin "initiates" the tumorigenic process. The "initiated" tissue foci may then be "promoted" to the visible tumor stage by weekly application of a promoting agent such as croton oil which alone is noncarcinogenic or weakly so. The "initiation" stage is irreversible since the onset of promotion can be delayed for long periods without diminution of tumor yield. Since "initiation" does not require the continuous application of carcinogen, and the single dose of carcinogen rapidly disappears from the skin, the system appears particularly useful for the biochemical analyses of the early events in chemical carcinogenesis. In this system, the susceptible tissue is also observable grossly and can be treated directly with the carcinogen as well as with other agents of known biological activity. The ability to apply agents directly minimizes systemic dilution and metabolism of the active agent. This system has been used to study the effects of a variety of chemical agents on chemical carcinogenesis. Thus, several workers2 have studied the effects of prolonged treatment with SH inhibitors on various stages of the process of skin tumorigenesis. In a previous report,3 we found that actinomycin D, an inhibitor of DNA-dependent RNA synthesist inhibited skin tumorigenesis when applied on the same day as the carcinogen. In -that study, the skin tumors were induced by small doses of DIMBA followed by weekly treatment with croton oil. An observation which may be related to our results is that of Burdette5 who has shown an inhibition by actinomycin D of both the lethal mutation frequency and the appearance of melanotic atypical growth induced by radiation in Drosophila melanogaster. In this study we investigated the effects of actinomycin D, applied at various intervals before and after DMBA, on subsequent tumor formation. This technique enabled us to examine the time required for the "initiation" process to be completed. In addition we also report on the effect of actinomycin D on skin tumorigenesis induced by large single doses of DMBA with no subsequent croton oil treatment and on urethan (ethyl carbamate)-initiated, croton oil-promoted skin tumorigenesis.

Inhibition of mouse skin tumorigenesis by actinomycin D.