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Study uncovers 'significant' functional differences of novel estrogen receptor

Because of these differences, this new estrogen receptor could become an important therapeutic target and may play a further signaling role in other estrogen target tissues, including uterus and prostate tissues.

These new findings could significantly advance the understanding of the effects of estrogen in breast cancer and point the way towards new and potentially more effective treatments of the disease.

The new study was published this week in an advanced online edition of the Proceedings of the National Academy of Sciences.

Estrogen has long been linked to the development of breast cancer, both through the stimulation of breast cell growth, which can lead to mutation, and through estrogen metabolism, which can interfere with apoptosis and DNA repair. Estrogen receptors mediate the majority of the actions of estrogen, including the metastatic growth of breast cancer cells, and are an important marker in therapy; readable levels of estrogen receptor proteins are expressed in a large portion of human breast cells.

Professor Thomas F. Deuel, M.D., a Scripps Research scientist who participated in the study said, "The estrogen and anti-estrogen signaling pathways mediated by this new receptor could explain why some breast cancers grow worse or become resistant to anti-estrogen therapy, specifically the drug tamoxifen, which blocks estrogen signaled responses through ER-a66 in breast tissue." According to the National Cancer Institute, anti-estrogen therapy is most often used in postmenopausal women whose tumors grow in response to the hormone.

"Worldwide, breast cancer is the most common form of cancer in women and the second most common cause of death for women in the United States," Deuel said. "The toll in suffering and mortality is especially devastating because breast cancer strikes women at a time in their lives when they are most productive and they are busy with children and raising a family. This continues despite g
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
9-Jun-2006


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