© The Author 2006. Published by Oxford University Press.
EDITORIAL |
Pak up Your Breast Tumor—and Grow!
Correspondence to: V. Craig Jordan, OBE, PhD, DSc, Vice President and Research Director of Medical Sciences, Fox Chase Cancer Center, 333 Cottman Ave., Philadelphia, PA 19111 (e-mail: v.craig.jordan@fccc.edu).
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The estrogen receptor (ER) has proved to be an extremely important target for the treatment of breast cancer (1). Tamoxifen, a nonsteroidal antiestrogen, blocks estrogen-stimulated breast cancer growth by binding to ER. However, years of adjuvant tamoxifen therapy are required to "smother" estrogen-sensitive micrometastases. Thus, two principles for optimal molecular therapeutics in breast cancer have emerged: tumor targeting and the appropriate duration of treatment that creates optimal survival advantages for patients (2). Although these principles have taken two decades to translate from the laboratory (3) to changes in healthcare (4), the widespread use of tamoxifen is credited with contributing substantially to the decline in death rates from breast cancer in the United States (5). Most importantly, in these days of meteoric rises in health care costs for targeted therapies, tamoxifen is, by contrast, a cheap and
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  K. Lehnes, A. D. Winder, C. Alfonso, N. Kasid, M. Simoneaux, H. Summe, E. Morgan, M. C. Iann, J. Duncan, M. Eagan, et al. The Effect of Estradiol on in Vivo Tumorigenesis Is Modulated by the Human Epidermal Growth Factor Receptor 2/Phosphatidylinositol 3-Kinase/Akt1 Pathway Endocrinology, March 1, 2007; 148(3): 1171 - 1180. [Abstract] [Full Text] [PDF]
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