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V. Craig Jordan, Pak up Your Breast Tumor—and Grow!, JNCI: Journal of the National Cancer Institute, Volume 98, Issue 10, 17 May 2006, Pages 657–659, https://doi.org/10.1093/jnci/djj204
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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 affordable drug that is known to save lives. However, because not all ER-positive breast cancers respond to tamoxifen treatment, the development of ways to improve targeting tamoxifen to treat the “right” tumors would be of value throughout the world.