Progestin effects on growth in the human breast cancer cell line T-47D--possible therapeutic implications |
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Authors: | J R Hissom M R Moore |
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Affiliation: | 1. Department of Chemistry, Faculty of Science, Srinakharinwirot University, Bangkok 10110, Thailand;2. Center of Data Mining and Biomedical Informatics, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand;3. Department of Community Medical Technology, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand;4. Department of Clinical Chemistry, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand;5. Laboratory of Medicinal Chemistry, Chulabhorn Research Institute, and Program in Chemical Biology, Chulabhorn Graduate Institute, Bangkok 10210,Thailand;6. Center of Excellence on Environmental Health and Toxicology, Commission on Higher Education (CHE), Ministry of Education, Thailand;7. Department of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Bangkok 10700, Thailand;1. Department of Pediatrics, Emory University, 2015 Uppergate Dr., Rm 426I, Atlanta, GA 30322, United States;2. Aflac Cancer and Blood Disorders Center, Children''s Healthcare of Atlanta, 2015 Uppergate Dr., Rm 426I, Atlanta, GA 30322, United States;3. Department of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, PO Box 19024, Seattle, Washington 98109, United States;4. Department of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, PO Box 19024, Seattle, Washington 98109, United States;5. Department of Pediatrics, Stanford University, 750 Welch Road, Suite 317, Palo Alto, CA 94304, United States;6. Department of Neurology, Stanford University, 750 Welch Road, Suite 317, Palo Alto, CA 94304, United States;7. Department of Human Biology, Stanford University, 750 Welch Road, Suite 317, Palo Alto, CA 94304, United States;8. Department of Epidemiology and Cancer Control, St. Jude Children''s Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN 38105, United States;9. Department of Psychology, St. Jude Children''s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, United States;10. Department of Medicine, Duke University School of Medicine, 2424 Erwin Dr., Suite 601, Durham, NC 27705, United States;11. Department of Oncology, St. Jude Children''s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, United States;12. Division of Haematology, Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada;13. Division of Oncology, Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada;14. Department of Paediatrics, University of Toronto, 555 University Avenue, Toronto, ON M5G 1X8, Canada;15. Department of Health Policy, Management, and Evaluation, University of Toronto, 555 University Avenue, Toronto, ON M5G 1X8, Canada;1. Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, Lanzhou, 730000, China;2. Medical Experimental Center, Lanzhou University, Lanzhou, 730000, China;1. Hematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy;2. Venetian Institute of Molecular Medicine, Centro di Eccellenza per la Ricerca Biomedica Avanzata, Padua, Italy |
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Abstract: | In order to determine growth effects of the progestin R5020, (promegestone), we have utilized the progesterone-receptor rich human breast cancer cell line T-47D, growing the cells in the absence of the pH indicator phenol red, which has recently been found to be estrogenic. In contrast to reports on cells grown in the presence of phenol red, we find that promegestone alone, at physiological progestin concentration, significantly stimulates growth. Estradiol alone, at physiological concentration, stimulates growth much more. Promegestone in combination with estradiol is antiestrogenic for growth; that is, it significantly decreases the growth stimulatory effect of estradiol. These results raise the possibility that estrogen receptor and progesterone receptor-rich breast cancer patients might benefit more from a combination of anti-progestin and anti-estrogen therapy than from anti-estrogens alone. |
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