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[Cancer Research 31, 1111-1117, August 1, 1971]
© 1971 American Association for Cancer Research

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Effect of Fluphenazine HCl on R3230AC Mammary Carcinoma and Mammary Glands of the Rat1

Russell Hilf2, Carlton Bell, Harold Goldenberg and Inge Michel

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.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1971 by the American Association for Cancer Research.