Cancer Letters, zyxwvutsrqponmlkjihgfedcbaZYXWVUTSRQPONMLKJIHGFEDCB 11 (1960) 57-61 0 ElsevierINorth-Holland Scientific Publishers Ltd. 57 HIGH DOSE ESTROGEN RESPONSE OF THE HORMONE INDEPENDENT R3327-At COPENHAGEN RAT PROSTATIC TUMOR* W.D.W. HESTON and D.W. LAZAN The Division of Urology, W ashington University School of Medicine, St. Louis, Missouri 631 IO (U.S.A.). (Received 30 October 1979) (Accepted 22 July 1980) - SUMMARY In studies with the hormone independent R3327-At prostatic tumor, relatively high doses of estrogen were inhibitory to the growth of the R3327- At rat prostatic tumor were observed. It was further observed that although tumor growth was inhibited, an increase in the [ 3H] thymidine labelling of the DNA of the tumor cells of the estrogen treated group relative to the castrate control was apparent. INTRODUCTION One of the few animal tumor models of prostatic carcinoma is the Copen- hagen rat prostatic tumor R3327 and its derivative lines [3,5,8]. During initial investigations on the slow growing and androgen-dependent well differentiated R3327-H tumor, there arose a rapidly growing anaplastic tumor which grew nearly equally well in intact or castrated males. This rapidly growing hormone independent derivative was designated R3327-At [ 61. While both androgen and estrogen receptors were present in the R3327-H tumor, none have been found in the R3327-At tumor, correlating to its lack of hormone responsiveness [ 5,6]. The hormone responsive tumor indicated reduction in its growth potential when treated with daily doses of estrogen of 0.1 mg/kg body wt. No effect of estrogen was found on the growth of the anaplastic R3327-At tumor at this dose level; however, when the daily dosage of diethylstilbestrol was increased 200-fold to 20 mg/kg body wt, the growth of this hormone insensitive tumor was inhibited. Our preliminary findings on this high dose estrogen effect on the hormone insensitive R3327- At prostatic tumor are presented. *Supported in part by Public Health Service grant CA23665 from the National Cancer Institute, National Institutes of Health, Education and Welfare.