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[Cancer Research 46, 1920-1927, April 1, 1986]
© 1986 American Association for Cancer Research

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Heterogeneity in the Hormonal Responsiveness of Clones Derived from the 13762NF Rat Mammary Tumor1

Joseph Geradts, James Richards2, Marc Edery, Kevin Pang, Lisa Larson and Satyabrata Nandi

Cancer Research Laboratory and Department of Zoology, University of California, Berkeley, California 94720

The transplantable hormone-responsive rat mammary adenocarcinoma 13762NF was dissociated with collagenase and hyaluronidase. Cells were cloned directly or lines were established from mass cultures and cells from these lines were cloned. Clones differed in cellular morphology, colony morphology on plastic or in collagen gel, growth rate, growth response to hormones, and hormone receptor levels. Growth response to prolactin, estradiol, progesterone, cortisol, and epidermal growth factor (EGF) was determined by culturing the cells within collagen gel and using a serum-free medium base of DME/F12 (1:1) with insulin, linoleic acid, and BSA. The clones varied in their hormone responses, with all 20 of the clones tested responding to cortisol in combination with EGF. Somes clones would respond to EGF, cortisol, or progesterone when used alone. None of the clones tested could be stimulated by prolactin or estradiol. Receptor levels for estradiol, progesterone, glucocorticoids, and EGF were assessed in 3 selected clones differing in their hormone responsiveness. Receptor levels appeared to correlate with hormonal sensitivity. Selected clones transplanted into female F344 rats produced carcinomas with histopathologies similar to the original tumor.

1 Supported by Grant No. CA05388, awarded by the National Institutes of Health, Department of Health and Human Services.

2 To whom requests for reprints should be addressed.

Received 6/18/85. Revised 12/23/85. Accepted 12/30/85.




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P. Buse, S. H. Tran, E. Luther, P. T. Phu, G. W. Aponte, and G. L. Firestone
Cell Cycle and Hormonal Control of Nuclear-Cytoplasmic Localization of the Serum- and Glucocorticoid-inducible Protein Kinase, Sgk, in Mammary Tumor Cells. A NOVEL CONVERGENCE POINT OF ANTI-PROLIFERATIVE AND PROLIFERATIVE CELL SIGNALING PATHWAYS
J. Biol. Chem., March 12, 1999; 274(11): 7253 - 7263.
[Abstract] [Full Text] [PDF]




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 © 1986 by the American Association for Cancer Research.