This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hilf, R. Articles by Carrington, M. J. Search for Related Content PubMed PubMed Citation Articles by Hilf, R. Articles by Carrington, M. J.

Influence of Endocrine Organ Ablation on the Growth and Biochemical Responses of the R3230AC Mammary Tumor to Hormonal Treatment¹

Squibb Institute for Medical Research, New Brunswick, New Jersey

Growth of the R3230AC mammary carcinoma was not altered by ovariectomy or orchiectomy of the tumor-bearing animal, when surgical ablation was performed prior to or at various times after transplantation of the neoplasm. Estradiol valerate treatment inhibited tumor growth in intact or gonadectomized hosts. This inhibition of tumor growth was accompanied by increases in tumor RNA/DNA ratios and elevations in the activities of glucose-6-phosphate dehydrogenase, malate dehydrogenase (decarboxylating), and phosphoglucomutase. Prolactin administered simultaneously with estrogen did not enhance the tumor growth inhibition observed with estrogen alone, but the combination treatment did augment the estrogen-induced enzyme activity increases in the tumors from ovariectomized hosts. Hypophysectomy reduced tumor growth, and estrogen treatment of the hypophysectomized tumor-bearing animal had no further effect on growth of the neoplasm. However, estradiol valerate did induce elevations in the activities of the above enzymes in the tumors of these hypophysectomized animals. Prolactin appeared to antagonize the estrogen-induced enzyme changes in these operated animals. Testosterone propionate, which inhibited the enzyme activities in the tumors from intact and orchiectomized animals, had no effect on tumor growth. Androgen treatment did inhibit growth of the carcinoma in ovariectomized animals, this inhibition being accompanied by elevations in glucose-6-phosphate dehydrogenase activity and RNA/DNA ratio in the neoplasm. These data are discussed in relationship to the role of these hormones in mammary cancer.

¹ Work supported by Contract Nos. SA-43-ph-2395 and PH43-65-1050 from the Cancer Chemotherapy National Service Center, National Cancer Institute, NIH, Bethesda, Maryland.

Received 11/12/65.