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Submitted on February 26, 2007
Accepted on April 11, 2007
Departments of Medicine, Microbiology, Physiologyand the Cancer Center, University of Virginia Health System, PO Box 800578, Charlottesville, VA 22908
* To whom correspondence should be addressed. E-mail: cms3e{at}virginia.edu.
The signaling pathways that are critical to the development and growth of breast cancer include those activated downstream of the estrogen receptor (ER) and the human epidermal growth factor receptor (HER) family. Many of these pathways, including the signal transducer and activator of transcription (STAT) pathway, are common to both. The well-described genomic actions of ER involve its role as a transcription factor, either by binding directly to DNA through estrogen response elements (EREs), or by tethering to DNA through interaction with other proteins. Non-genomic signaling by the ER involves interaction with membrane-associated signaling proteins such as the c-Src tyrosine kinase and adapter proteins p130Cas and moderator of non-genomic activity of estrogen receptor (MNAR). Interactions with the STAT pathway are important in both ER signaling pathways and are critical for estrogen-induced proliferation and tumorigenesis. These mechanisms of signaling crosstalk and their role in resistance to anti-estrogen therapies are discussed.
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