Cortisone and Carcinogenesis in Mouse Skin

It has been demonstrated that cortisone may enhance the development of metastases in both transplanted and spontaneous experimental tumors (2, 5, 7, 8). Whether or not this effect is the result of alterations in the primary tumor, the tumor bed, the sites of metastases, or is systemic is not clear. Furthermore, contradictory results have been reported concerning the effects of cortisone on the action of carcinogens in mice. Both a lowered incidence of tumor production (4, 10) and an increased incidence (11) have been reported. However, the experimental procedures have not been identical. There have been variations in the strain of mice, the dose of cortisone and duration of its administration, the number of times the carcinogen was painted, and the nature of the carcinogen used. Conflicting findings have also been reported concerning the role of the pituitary gland in experimental skin carcinogenesis (1, 9). To gain further information about the role of the pituitary-adrenal axis, and particularly about cortisone, relative to experimental tumor production and metastases, and in an attempt to reconcile some of the conflicting observations, a series of experiments utilizing cortisone and methylcholanthrene have been instituted. In these studies cortisone is being administered during the early phases of methylcholanthrene painting, during the entire latent period, continuously throughout the course of tumor growth, or only after the appearance of papillomas. The number of paintings is also being varied. This report concerns the first of these completed studies.