The effect of cortisone and hair cycle on the incidence of chemically induced epidermal tumors in mice.

In previous communications we reported that under certain experimental conditions systemic cortisone administration accelerated the occurrence of chemically induced epidermal tumors in mice (15-17, 30, ~6). The results were confirmed by Spain, Molomut, and Novikoff (95). We postulated that this effect is caused by an inhibitory influence of the steroid on hair follicular growth (15-17, 34). This assumption was based (a) on our own observation that subcutaneous cortisone injections inhibit hair follicular growth and thus protract hair follicular rest in mice (which was in line with similar observations made by Baker et al. in rats [3, 8, 11, 37, ~8]) and (b) on the observation made almost simultaneously by Scandinavian investigators (1, 5) and by Cowdry's group (18) that chemically induced epidermal tumors more readily develop when exposure to the carcinogen occurs during the resting phase of the hair cycle than when it occurs during the growing phase. Two large-scale experiments conducted a few years ago to prove the validity of our hypothesis failed to yield any conclusive results, because of shortcomings in the procedure. A new hair cycle was initiated artificially in these experiments by plucking of the fur. In both experiments one group of the animals was subjected to a single exposure to the carcinogen (dimethylbenzanthracene) during the growing phase--anagen--of the hair cycle, whereas a second group was subjected to the same exposure during the resting phase--telogen--of the cycle. About half of each group of mice received cortisone injections at the time of the carcinogen exposure, while the other half (controls) did not receive any cortisone. According to our theory, a higher tumor incidence was expected to occur in