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Studies on the Mechanism of Skin Tumor Promotion¹

McArdle Laboratory for Cancer Research, University of Wisconsin Medical Center, Madison, Wisconsin 53706

At a level which was effective as a skin tumor promoter, croton oil increased the rate of incorporation of tritiated precursors into mouse skin macromolecules. After a single application of croton oil, the early 2- to 3-fold stimulation of RNA and protein synthesis and the 60% inhibition of DNA synthesis was followed by a 3-fold stimulation of DNA synthesis at 18 hr. The rates of macromolecular synthesis returned to normal levels within 7 days. A single application of cantharidin, a weak tumor promoter, stimulated both DNA and RNA synthesis in mouse skin. Treatment with either croton oil or cantharidin stimulated the synthesis of rapidly labeled RNA when measured 2 hr after treatment; stimulation of RNA synthesis may be important in the process of promotion. When an incision was made in initiated skin, tumors developed along the line of wound healing. Because croton oil, cantharidin, and other promoters cause hyperplasia and because wound healing causes a local stimulation of mitosis, a stimulation of cell division may be involved in promotion. A possible molecular mechanism of skin carcinogenesis is discussed.

¹ This work was supported in part by grants from the Alexander and Margaret Stewart Trust Fund, the American Cancer Society (E-6K), and the National Cancer Institute (CA-07175 and CA-05002).

Received 8/29/68. Accepted 6/ 4/69.

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