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 Bogden, A. E. Articles by Speropoulos, A. Search for Related Content PubMed PubMed Citation Articles by Bogden, A. E. Articles by Speropoulos, A.

The Effect of Perphenazine-induced Serum Prolactin Response on Estrogen-primed Mammary Tumor-Host Systems, 13762 and R-35 Mammary Adenocarcinomas¹

Department of Immunobiology, Mason Research Institute, Worcester, Massachesetts 01608 [A. E. B., E. Y. H. K., M. M. M., A. S.], and Endocrine Evaluation Branch, Division of Cancer Biology and Diagnosis, National Cancer Institute, NIH, Bethesda, Maryland 20014 [D. J. T.]

The effect of perphenazine, a phenothiazine derivative, on serum prolactin levels, on maturation of the normal mammae, and on growth of mammary adenocarcinomas was studied using two transplantable rat mammary tumor systems, the 13762 mammary tumor (13762 MT) in the syngeneic Fischer 344 strain and the R-35 mammary tumor (R-35 MT) in allogeneic Sprague-Dawley stock. Perphenazine induced a dose-response increase in the serum prolactin levels of both normal and tumor-bearing animals and stimulated maturation of the normal mammae. The resultant responses of the two mammary tumors to perphenazine treatment were in exact contrast. Growth of the 13762 MT was accelerated whereas growth of the R-35 MT was inhibited. There was atrophy of the mammae and a concomitant decrease in serum prolactin levels in young, sexually maturing females with progressively growing 13762 MT tumors. Normal mammae and serum prolactin levels were unaffected in similar females bearing the R-35 MT. Treatment of the hosts with estrogen prior to tumor implantation, as well as treatment of both tumor and host, enhanced the effects of perphenazine on serum prolactin levels, on the normal mammae, and on mammary tumor growth, i.e., stimulation of 13762 MT and inhibition of R-35 MT.

¹ This investigation was supported by Contract PH43-65-6 from the Endocrine Evaluation Branch, General Laboratories and Clinics, National Cancer Institute, NIH.

Received 12/14/72. Accepted 8/ 2/74.