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Chapter 086. Breast Cancer (Part 10)

Endocrine Therapy Normal breast tissue is estrogen-dependent. Both primary and metastatic breast cancer may retain this phenotype. The best means of ascertaining whether a breast cancer is hormone-dependent is through analysis of estrogen and progesterone receptor levels on the tumor. Tumors that are positive for the estrogen receptor and negative for the progesterone receptor have a response rate of ~30%. Tumors that have both receptors have a response rate approaching 70%. If neither receptor is present, the objective response rates are . | Chapter 086. Breast Cancer Part 10 Endocrine Therapy Normal breast tissue is estrogen-dependent. Both primary and metastatic breast cancer may retain this phenotype. The best means of ascertaining whether a breast cancer is hormone-dependent is through analysis of estrogen and progesterone receptor levels on the tumor. Tumors that are positive for the estrogen receptor and negative for the progesterone receptor have a response rate of 30 . Tumors that have both receptors have a response rate approaching 70 . If neither receptor is present the objective response rates are 10 . Receptor analyses provide information as to the correct ordering of endocrine therapies as opposed to chemotherapy. Because of their lack of toxicity and because some patients whose receptor analyses are reported as negative respond to endocrine therapy an endocrine treatment should be attempted in virtually every patient with metastatic breast cancer. Potential endocrine therapies are summarized in Table 86-4. The choice of endocrine therapy is usually determined by toxicity profile and availability. In most patients the initial endocrine therapy should be an aromatase inhibitor rather than tamoxifen. For the subset of women who are ER positive but also HER-2 neu positive response rates to aromatase inhibitors are very substantially higher than to tamoxifen. Newer pure antiestrogens that are free of agonistic effects are also in clinical trial. Cases in which tumors shrink in response to tamoxifen withdrawal as well as withdrawal of pharmacologic doses of estrogens have been reported. Endogenous estrogen formation may be blocked by analogues of luteinizing hormone-releasing hormone in premenopausal women. Additive endocrine therapies including treatment with progestogens estrogens and androgens may also be tried in patients who respond to initial endocrine therapy the mechanism of action of these latter therapies is unknown. Patients who respond to one endocrine therapy have at least a 50 .