Inhibition of a transplantable pancreatic carcinoma by castration and estradiol administration in rats.
Influence of sex steroids on the growth of an azaserine-induced transplantable rat pancreatic carcinoma, DSL-2, was studied. This established transplantable tumor has been maintained in syngeneic rats. Inbred male Lewis rats were pretreated with castration and s.c. implantation of 1.0-mg 17 beta-estradiol (CAS: 50-28-2; estradiol) pellets at 7 weeks of age. Tumor cells were inoculated s.c. on the back of intact male, castrated male, or 17 beta-estradiol-treated castrated male rats. Additional male rats served as non-tumor-bearing controls. There was no difference in the body weight between tumor-bearing and non-tumor-bearing male rats. A distinct difference in the tumor growth was observed in variously conditioned recipients. In castrated male hosts, the serum testosterone levels and the epididymis weights were significantly decreased, and the tumor weights were significantly less as compared to intact control hosts. Additional pretreatment with 17 beta-estradiol caused a markedly slower growth of tumors and increases of the serum 17 beta-estradiol levels and the pituitary weights in castrated male recipients. The remarkable response of tumor growth to castration was also observed in a fast-growing tumor derived from DSL-2. Moreover, close positive relationships between tumor weights and the activities of both serum amylase and lipase were observed. Results showed that the pretreatment with castration alone or in combination with 17 beta-estradiol treatment was able to inhibit the growth of the transplantable tumor. In addition, tumor cells had an ability to produce amylase and lipase, and the amount of enzymic activity was related to the tumor volume. Thus, these data indicate that the transplantable rat pancreatic carcinoma retains physiological function. Our previous study has shown the modulation by sex steroids of azaserine-induced preneoplastic lesions of pancreas in rats. Therefore, androgens and estrogens may play key roles as promoters and inhibitors during the process of pancreatic carcinogenesis.
Sumi
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Department of Pathology, Dartmouth Medical School, Hanover, New Hampshire 03756.
Brinck-Johnsen
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Longnecker
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D000681:Amylases / Q000097:blood; D002277:Carcinoma / Q000628:therapy*; D003131:Combined Modality Therapy; D004958:Estradiol / Q000494:pharmacology*; D008049:Lipase / Q000097:blood; D008297:Male; D009368:Neoplasm Transplantation; D009919:Orchiectomy; D010190:Pancreatic Neoplasms / Q000628:therapy*; D013739:Testosterone / Q000097:blood
D013739:Testosterone; D004958:Estradiol; D008049:Lipase; D000681:Amylases