Antitumourigenic Action of Steroids as an ‘Independent’ Faculty of these Compounds

Abstract

As the power of steroids to prevent œstrogen-induced abdominal fibroids decreases with their diminishing progestational activity (progesterone → deoxycorticosterone → testosterone), we assumed, in an earlier phase of our work, that antifibromatogenic activity is correlated with the progestational one¹. Whereas the finding that the non-progestational δ¹⁶-dehydroprogesterone was not antifibromatogenic seemed to substantiate this assumption, subsequent statements of ours were contrary to it. It has long been known that substitutions at C₁₇ considerably increase the progestational activity of testosterone²; however, when ethinyl-, ethyl- and vinyl-testosterone were tried in our work with fibroids, they were found to be not more, and often even less, antifibromatogenic than testosterone^3,4. Similarly, there was no correlation between androgenic and antifibromatogenic activities. Neither was there any correlation between cortical and antifibromatogenic activities. Pregnenolone-3-acetate is much inferior to 21-acetoxypregnenolone in maintaining alive the suprarenalectomized guinea pig₅; however, very large quantities of the former prevented the formation of fibroids, whereas this was not the case with similar quantities of the latter⁶. Thus we reached the conclusion that antifibromatogenic activity is a faculty per se, not a sequel of any known, or classical, physiological action of the respective steroids^4,7. It is not ‘subordinate’ to progestational action; it is an ‘independent’ action, to use Selye's⁸ terminology.