Abstract
Successful endocrine therapy in breast cancer has been theorized to be dependent upon retention by the tumor of at least part of the cell’s differentiated endocrine functions (1). Estrogen receptors (ER) therefore have been measured extensively in breast tumor biopsies in numerous laboratories as a potential marker of a functional endocrine system. Accordingly, tumors containing ER are much more likely to respond to endocrine therapies than tumors without ER (2). ER alone however is not a totally reliable marker of tumor sensitivity to hormones since certain tumors containing ER do not respond to endocrine manipulations. This is not surprising however, considering that binding of the hormone to the estrogen receptor is only the first step in a complex biochemical pathway leading to the physiological effect of estrogens (3). Any number of points in the pathway may conceivably be missing or defective. For this reason, we hypothesized that an end product of estrogen stimulation would improve the reliability of ER as a marker of hormone-responsive tumor growth (4). Progesterone receptor (PgR) is a likely candidate since it has been shown to be regulated by estrogens in animal mammary tumor models (5, 6) and in human breast cancer cells in tissue culture (7). Simultaneous measurement of PgR and ER in fact does improve the reliability of ER measurement alone in predicting patient response to endocrine therapies (8).
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© 1982 Plenum Press, New York
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Edwards, D.P., Adams, D.J., McGuire, W.L. (1982). Estrogen Regulation of Growth and Specific Protein Synthesis in Human Breast Cancer Cells in Tissue Culture. In: Leavitt, W.W. (eds) Hormones and Cancer. Advances in Experimental Medicine and Biology, vol 138. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-7192-6_8
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DOI: https://doi.org/10.1007/978-1-4615-7192-6_8
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