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Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030
* To whom correspondence should be addressed. E-mail: suzannef{at}breastcenter.tmc.edu.
As early as the 1800's the actions of estrogen have been implicated in the development and progression of breast cancer. In the late 1950's the estrogen receptor (ER) was identified, and subsequently purified a few years later. However, it was not until the 1980's that the first ER was molecularly cloned, and then in the mid 1990's, a second ER was cloned. These two related receptors are now called ER
and ER
, respectively. Since their discovery, much research has focused on identifying alterations within the coding sequence of these receptors in clinical samples. As a result, a large number of naturally-occurring splice variants of both ER and ER have been identified in normal epithelium, and diseased or cancerous tissues. In contrast, only a few point mutations have been identified in human patient samples from a variety of disease states, including breast cancer, endometrial cancer, and psychiatric diseases. To elucidate the mechanism of action for these variant isoforms or mutant receptors, experimental mutagenesis has been used to analyze the function of distinct amino acid residues in the ERs. This review will focus on ER and ER alterations in breast cancer.
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