The effect of cortisone on the induction and development of hamster-pouch carcinomas

Abstract

T he role of cortisone and various steroid hormones in experimental carcinogenesis has presented problems in interpretation, since a diversity of experimental results have been reported. An augmentation of the action of carcinogenic chemical agents was reported by Sulzberger and associates1 and by Spain, Molomut, and Novikoff.* A depression of the action of carcinogenic substances was reported by Engelbreth-Holm and Asboe-Hansen3 as well as by Ghadially and Green4 Gillman, Hathorn, and Penn5 reported no significant effect of cortisone on chemically induced neoplasms in experimental animals. Sabes, Chaudhry, and Gorli+ reported an increased yield of chemically induced buccal-pouch carcinomas in hamsters in which cortisone was applied topically. However, these authors found depressed tumor induction in the submandibular gland when cortisone was injected locally. Anbari, Shklar, and Cataldo’ found that systemically administered cortisone resulted in an augmentation of the action of a chemical carcinogen on rat submandibular glands, so that tumor-induction time was decreased and a larger number of carcinomas developed. I have recently reported an increased incidence of chemically induced buccal-pouch carcinomas in hamsters that had also received injections of cortisone.8 In addition to its effect on carcinogenesis, cortisone has also been reported to induce metastases of transplanted mouse tumors9 and to facilitate the growth of human carcinomas in experimental animals.‘0 Since the implication that a corticosteroid hormone could have a cocarcinogenic influenceI was of considerable significance, it was thought that a detailed histologic study of the induced neoplasms in cortisone-injected and control animals was indicated. Histopathologic observations would reveal the sequence of