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[Cancer Research 49, 6295-6299, November 15, 1989]
© 1989 American Association for Cancer Research

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Antiestrogen Inhibition of Prolactin-induced Growth of the Nb2 Rat Lymphoma Cell Line

Ratna Biswas and Barbara K. Vonderhaar1

Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892

The rat lymphoma cell line Nb2 is highly prolactin responsive in terms of growth. Estrogens are without effect in these cells that lack the estrogen receptor. The growth stimulation by lactogenic hormones is effectively inhibited by antiestrogens, such as tamoxifen and nafoxidine, at concentrations as low as 10-10 M. The growth inhibition is partially reversed by replacement of the antiestrogens by prolactin. Nb2 cells contain estrogen-noncompetitive specific antiestrogen binding sites on their membranes that bind tamoxifen with an average Kd of 3.1 x 10-10 M. Addition of antiestrogens to the binding reaction inhibits lactogenic hormone binding to membrane-bound receptors. The order of affinities of various antiestrogens (tamoxifen, nafoxidine, 2-(4-tert-butyl-phenoxy)ethyl diethylamine hydrochloride, and LY117018) for the antiestrogen binding sites parallels the order of their potencies as growth and lactogen binding inhibitors. These data suggest that antiestrogens, possibly acting through the antiestrogen binding sites, may function as antilactogens.

1 To whom requests for reprints should be addressed, at NIH, Bldg. 10, Room 5B56, Bethesda, MD 20892.

Received 5/15/87. Revised 12/31/89. Revised 8/ 8/89. Accepted 8/16/89.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1989 by the American Association for Cancer Research.