The present study compared the ability of 12-O-tetradecanoylphorbol-13-acetate (TPA) and
teleocidin to induce sustained epidermal
hyperplasia, activate partially purified epidermal
protein kinase C (PKC)
isozymes and promote skin
tumors in SENCAR and C57BL/6 mice.
Teleocidin was less effective than TPA on a molar basis for inducing sustained epidermal
hyperplasia, promoting skin
tumors and activating partially purified epidermal PKC
isozymes in vitro when examined using SENCAR mice. In contrast,
teleocidin was more effective than TPA on a molar basis for inducing sustained epidermal
hyperplasia, approximately equi-effective for promoting skin
tumors and significantly less effective for activating PKC
isozymes in vitro when examined using C57BL/6 mice. Despite the differences in response of C57BL/6 mice to TPA and
teleocidin, this mouse strain was still highly resistant to skin
tumor promotion by both types of promoters when compared with SENCAR mice. The current results, when considered in light of our recent studies (
Cancer Res., 51, 1398-1405, 1991), indicate that C57BL/6 are generally resistant to a variety of classes of skin
tumor promoters, including the
teleocidins. In addition, except for the
phorbol esters, the induction of sustained epidermal
hyperplasia does not appear to be as good a marker for overall promotion responsiveness between SENCAR and C57BL/6 mice with other classes of
tumor promoters; although the induction of a significant sustained
hyperplasia in the latter mouse strain did yield a weak
tumor response. Taken together, the current data suggest that factors in addition to the induction of sustained epidermal
hyperplasia, control responsiveness of C57BL/6 mice to skin
tumor promotion by diverse promoting stimuli.