Abstract
Over 30 years of clinical data have unequivocally established estrogen receptor (ER)-α as a critical clinical biomarker and valid therapeutic target to fight breast cancer. However, ERα remains imperfect with respect to both of these activities, mainly because the mechanisms by which estrogens mediate their activity are far more complex than originally anticipated. The cloning of a second estrogen receptor, ERβ, has led to a full re-evaluation of our original view of the action of estrogen in breast tissues. Important challenges remain with respect to the design, selection and normalization of the most appropriate methods for assaying the expression and functionality of both receptors. Solving these challenges remains a priority in order to decide upon specific endocrine therapies and save patients who are still dying from a potentially curable disease.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.