ABSTRACT
In the late nineteenth century, Beatson reported on the response of advanced carcinoma of the breast to oophorectomy [1 J. These empirical observations led to additional radiotherapeutic and surgical methods of hormonal manipulation, including adrenalectomy and hypophysectomy [2~3]. The response rate to such endocrine ablations in patients with metastatic carcinoma of the breast was in the range of 30% [2,3]. It was not until the 1960's that Jensen and Jacobson demonstrated the binding of labeled estrogens to hormone-responsive target tissues [4]. In the same period, Folca et al. [5] observed in vivo binding of estrogen derivatives in hormonally responsive tumors, and Toft and Gorski succeeded in the extraction of a high-affinity steroid binding protein [6]. These observations gave experimental support to a model of hormonal action, mediated via specific steroid receptors, and led to the hypothesis that estrogen receptor-rich tumors would be responsive to endocrine manipulation, whereas receptor-poor tumors would not. In the past 25 years, numerous series have confirmed that breast carcinomas that contain estrogen receptors exhibit a predictable responsiveness to hormonal therapy [7-10]. However, the usefulness of the detection of estrogen receptors is not only that it relates to the latter point, but also defines a favorable prognosis group among all patients with breast carcinoma. Those with estrogen receptor-rich tumors have greater disease-free and overall survivals than others with receptor-poor carcinomas [11].
