Regression of experimental skin tumors in mice following local injections of 17-hydroxycorticosterone-21-acetate.

It was shown in 1953 by Engelbreth-Holm and Asboe-Hansen (4) that cortisone, injected intraperitoneally, caused a definite reduction in the de velopment of tumors and an increased latent pe riod in albino mice of strain ST/Eh painted once with 9,10-dimethyl-l,2-benzanthracene (DMBA). Similar results were obtained by Boutwell and Rusch (3) with carcinomas induced by benzpyrene. Sulzberger, Herrmann, Piccagli, and Frank (8) found that repeated subcutaneous injec tions of cortisone increased the incidence of skin tu mors induced by methylcholanthrene in albino mice of a Swiss strain. The adrenal cortical steroid cortisone is known to exert an effect on the fibroblasts (6, 7), on the ground substance, and the mast cells (1, 2, 9), and thus on the connective tissue as a whole. Only a few reports have been published on alterations in ectodermal tissues caused by adrenal cortical ster oids. Green and Ghadially (5) found that cortisone inhibited the mitotic activity in mouse epidermis. This did not, however, apply to epidermis painted with 9,10-dimethyl-],2-benzanthracene. In tu mors the mitoses were also found to be resistant. The connective tissue of skin tumors (precancerous papillomas) induced by 9,10-dimethyl-],2benzanthracene contains enormous quantities of mast cells (4). Their presence in the connective tis sue of tumors is worth noting, as mast cells are presumed to produce a ground-substance com ponent of the hyaluronic acid and heparin type which probably influences the permeability of the connective tissue (1, 2). The role of connective tissue in skin carcinogenesis still remains to be elucidated. However, since in systemic therapy cortisone has affected