Peroxidase activity as a marker for estrogenicity: studies in uterus and mammary tumors

We examined the possibility that peroxidase activity might be a marker for estrogen activity in established estrogen-dependent tissues: dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors and human breast cancer. In DMBA-induced tumors undergoing regression after ovariectomy or tamoxifen treatment, tumor size decreased by 50%, estradiol receptors (ER) and progesterone receptors (PgR) decreased by 25 and 20%, respectively, but peroxidase activity paradoxically increased six- to sevenfold. In DMBA tumors stimulated by estradiol treatment or by the cessation of tamoxifen administration in intact rats, tumor size increased threefold. ER and PgR increased two- and threefold, respectively, while peroxidase activity decreased 50%. These data indicate an inverse relation between tumor growth, ER and PgR on the one hand, and peroxidase activity on the other. In the human breast cancers there was a significant negative relation between the presence of ER and peroxidase activity. By using a calibrated Sephadex G-100 column it was shown that uterine peroxidase differs in molecular weight from the peroxidase of rat mammary tumors and that of human breast cancer.