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Notice: The authors and publisher have made every effort to ensure that the patient care recommended herein, including choice of drugs and drug dosages, is in accord with the accepted standard and practice at the time of publication. However, since research and regulation constantly change clinical standards, the reader is urged to check the product information sheet included in the package of each drug, which includes recommended doses, warnings, and contraindications. This is particular important with new or infrequently used drugs. Any treatment regimen, particularly one involving medication, involves inherent risk that must be weighed on a case-by-case basis against the benefits anticipated. The reader is cautioned that the purpose of this book is to inform and enlighten; the information contained herein is not intended as, and should not be employed as, a substitute for individual diagnosis and treatment.

An important application of the ER assay is the selection of appropriate patients for endocrine therapy. Approximately 50 to 60% of patients with ER-positive tumors benefit from endocrine therapy. 291, 292 This percentage includes patients who achieve a major objective remission (partial or complete) and those who derive long-term (> 6 months) stability of the disease with endocrine therapy; both groups have equivalent survival expectations. The ER status predicts equally well for all modalities of endocrine therapy. Patients with no detectable ER in their tumors do not benefit from endocrine therapy; however, patients with very low but detectable ER and/or PR respond, albeit infrequently, to endocrine therapy. 293 This may explain why some patients with “ER-negative” tumors have been reported to benefit from adjuvant tamoxifen therapy. It is not known why 40 to 50% of ER-positive tumors fail to respond to hormonal therapy despite the presence of receptor. Quantitative ER assay and the simultaneous determination of PR expression increase the predictive accuracy of these assays. Tumors with high ER concentration (> 100 fmol/mg protein or strong, homogeneous staining) or those positive for both ER and PR have the highest probability of response and clinical benefit from hormonal therapy. 294, 295 Tumor ER and PR status can change over time or with intervening therapy; thus, repeat biopsies of accessible tissue may be helpful in selecting sequential therapies. However, ER status on the primary tumor still predicts reasonably well for endocrine response at the time of relapse. Although there is a modest trend for higher response rate to chemotherapy in ER-negative patients, receptor status is not helpful in predicting response to chemotherapy. Clearly, an assay that would identify truly hormone-insensitive tumors would be more clinically useful. Variant and/or mutated ERs have been identified in breast cancer tissue. 296 Some of these altered receptors are constitutively active (activate transcription in the absence of estrogen), some are inactive, and some have dominant negative activity. The biologic importance of these variants and their role, if any, in hormone-resistant states remains to be clarified.

Decker steroid

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