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Squibb Institute for Medical Research, New Brunswick, New Jersey 08903
The administration of a phenothiazine tranquilizer, fluphenazine HCl, caused a decrease in the growth of the R3230AC mammary adenocarcinoma of the Fischer rat. Examination of various biochemical parameters in the cancers of fluphenazine HCl-treated animals showed that drug treatment caused a decrease in DNA levels, an increase in free fatty acids and triglycerides, and significant elevations in the activities of glucose-6-phosphate dehydrogenase, NADP-malate dehydrogenase, phosphoglucomutase, and aspartate aminotransferase. Mammary glands from the drug-treated tumor-bearing animals were stimulated and demonstrated striking increases (2 to 5 times per unit of tumor weight or 10 to 20 times per mg DNA) in enzyme activities compared with those found in control animals. The alterations reported were ascribed to the known ability of phenothiazines to stimulate endogenous secretion of prolactin. Thus, creating a hormonal milieu that stimulates normal mammary glands does not necessarily stimulate growth of mammary tumors.
1 Supported by Contract PH43-65-1050, Endocrine Evaluation Branch, General Laboratories and Clinics, National Cancer Institute, NIH, Bethesda, Md.
2 Present address: Biochemistry Department, University of Rochester School of Medicine and Dentistry, Rochester, N. Y. 14620.
Received 1/25/71. Accepted 4/ 8/71.
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