© 1995 by Oxford University Press
Journal of the National Cancer Institute, Vol. 87, No. 10, 746-750,
May 17, 1995
© 1995 Oxford University Press
Comparison of the Effects of a Pure Steroidal antiestrogen With Those of Tamoxifen in a Model of Human Breast Cancer
Department of Medicine, division of Medical Oncology, The University of Texas Health Science Center at San Antonio San Antonio, Tex
Zeneca Pharmaceuticals, Mereside Alderley Park Macclesfield, Cheshire, England, U.K.
Tenovus Cancer Research Center, University of Wales College of Medicine Heath Park, Cardiff, Wales, U.K.
Correspondence to: C. Kent Osborne, M.D., Department of Medicine, Division of Medical Oncology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284–7884.
Background: Tamoxifen, a non-steroidal estrogen antagonist, is the most prescribed drug for the treatment of breast cancer. The use of tamoxifen is limited, however, by the development of resistance to this compound in most patients. Although tamoxifen behaves primarily as an estrogen antagonist, it has agonist (or growth-stimulatory) activity as well. ICI 182, 780 is a 7
-alkyl-sulfinyl analogue of estradiol lacking agonist activity. The absence of agonist activity may make this steroidal antiestrogen superior to tamoxifen in suppressing tumor cell growth. Purpose: We compared the inhibitory effects of ICI 182, 780, tamoxifen, and estrogen withdrawal on the growth of established tumors and on tumorigenesis in a model system that uses estrogen-dependent, human MCF-7 breast tumor cells growing in athymic nude mice. We also studied the hormonal responsiveness of tumors that became resistant to the two estrogen antagonists and the effects of these drugs on estrogen-regulated gene expression. Methods: MCF-7 cells were injected subcutaneously into the flanks of castrated, female nude mice. The effects of repeated doses of tamoxifen and ICI 182, 780 (500 µg and 5 mg, respectively) on the growth of established tumors (8–10 mm in size) were determined after supplemental estrogen was removed. The effects of anti-estrogen treatments on the process of tumorigenesis, in the absence of estrogen supplementation, were determined by initiating drug administration on the same day as tumor cell inoculation. To evaluate the hormonal responsiveness of tumors resistant to tamoxifen and ICI 182, 780, 1-mm segments of the tumors were transplanted onto the flanks of new recipient mice, which were then treated with estrogen or the antiestrogens—alone or in combination. Tumor growth was monitored by measuring tumor volumes twice a week. Expression of the estrogen-responsive genes, pLIVl and pS2, in the tumors of treated animals was analyzed using blots of total cellular RNA and complementary DNA probes. Results: Treatment with ICI 182, 780 suppressed the growth of established tumors twice as long as treatment with tamoxifen or estrogen withdrawal. Tumorigenesis, in the absence of supplemental estrogen, was delayed to a greater extent in ICI 182, 780-treated mice than in tamoxifen-treated mice. ICI 182, 780 was found to be more effective than tamoxifen in reducing the expression of estrogen-regulated genes. Most tumors eventually became resistant to ICI 182, 780 and grew independently of estrogen. Conclusions: ICI 182, 780 is a more effective estrogen antagonist than tamoxifen in the MCF-7 tumor cell/nude mouse model system. [J Natl Cancer Inst 87: 746–750, 1995]
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H. Huynh, X. Yang, and M. Pollak Estradiol and Antiestrogens Regulate a Growth Inhibitory Insulin-like Growth Factor Binding Protein 3 Autocrine Loop in Human Breast Cancer Cells J. Biol. Chem., January 12, 1996; 271(2): 1016 - 1021. [Abstract] [Full Text] [PDF]
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J. S. Carroll, O. W. J. Prall, E. A. Musgrove, and R. L. Sutherland A Pure Estrogen Antagonist Inhibits Cyclin E-Cdk2 Activity in MCF-7 Breast Cancer Cells and Induces Accumulation of p130-E2F4 Complexes Characteristic of Quiescence J. Biol. Chem., December 1, 2000; 275(49): 38221 - 38229. [Abstract] [Full Text] [PDF]
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