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Medicine Branch [J. C. A., M. E. L., A. B., K. K. H., H. M. T. D., S. C. A., R. W.], Laboratory of Biochemistry [E. B. T.], and Biostatistics Section, Clinical Oncology Program [R. S.], National Cancer Institute, Bethesda, Maryland 20205, and Department of Oncology, Howard University, Washington, D. C. 20059 [L. G.]
The influence of steroid hormone receptors on response rate to endocrine therapy in 85 patients with metastatic breast cancer was determined in a retrospective study. We have previously reported that estrogen receptor status has an over-whelming influence on predicting response to therapy when compared to other prognostic variables. In the present study, we expand our analysis to include the results of progesterone, androgen, and glucocorticoid receptors. Of 18 patients whose tumors contained progesterone receptor, 11 responded to endocrine therapy, compared to 8 of 26 patients with low or absent progesterone receptor. Progesterone receptor increased the predictive index of the estrogen receptor in a group of patients who had received no prior therapy, but it did not help in patients who had received prior endocrine therapy. None of four patients whose tumors were estrogen receptor negative but progesterone receptor positive responded to endocrine therapy. At the present time, there are trends suggesting a possible association between androgen and glucocorticoid receptor and response to endocrine therapy. These trends are apparent only with a cutoff value of 10 fmol/mg cytoplasmic protein, and the distributions of androgen and glucocorticoid receptor values for responders and nonresponders are not significantly different. Knowledge of androgen receptor status does not increase the predictive index in estrogen receptor-positive tumors or estrogen receptor-negative tumors. Glucocorticoid receptor positivity may increase the predictive index in estrogen receptor-positive tumors, but not in estrogen receptor-negative tumors.
1 To whom requests for reprints should be addressed, at Building 10, Room 6B02, Medicine Branch, National Cancer Institute, NIH, Bethesda, Md. 20205.
Received 6/16/78. Accepted 2/21/79.
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