Mechanism of action of endocrine therapy Normal breast epithelial cells contain various hormone receptors such as estrogen receptor (ER) and progesterone receptor (PR). The normal development of the breast depends on the coordinated action of multiple hormones. After breast cancer, some breast cancer tissues can retain all or some of the hormone receptors and function, and their growth and development are influenced by the hormonal environment. Endocrine therapy is to inhibit the growth of breast cancer cells and treat breast cancer by inhibiting estrogen synthesis, lowering estrogen levels, blocking the binding of estrogen to its receptors, and partially or fully inhibiting the activity of estrogen receptors through the use of drugs or other means. Methods of endocrine therapy 1. Surgical debulking or drug debulking The site of estrogen production in the body is related to the menstrual status. In pre-menopausal women, estrogen is mainly produced by the ovaries; in post-menopausal women, the ovaries are atrophied and estrogen is mainly produced by peripheral tissues through the transformation of androgen precursors secreted by the adrenal glands by aromatase. In premenopausal patients with positive estrogen receptors, ovariectomy can inhibit tumor growth and improve survival rates. However, an increasing number of patients are now opting for pharmacologic ovarian debulking. The commonly used drug is Goserelin. 2. Tamoxifen TAM Tamoxifen TAM is the most commonly used endocrine therapeutic drug in clinical practice, and the general usage is 10mg per time, twice daily. Its main mechanism of action is to compete with estrogen to bind the intracytoplasmic estrogen receptor, forming TAM-receptor protein complex, which enters the nucleus and inhibits the synthesis of DNA and mRNA in cancer cells, thus inhibiting the proliferation of breast cancer cells. At present, it is considered that oral tamoxifen has the best effect for 5 years. 3.Aromatase inhibitors In premenopausal women, estrogen is mainly produced by aromatase in the ovaries. This enzyme can convert androgens into estrogen, and this process is controlled by follicle-stimulating hormone and luteinizing hormone in the pituitary gland. Under normal feedback loop regulation, estrogen secretion can be promoted by pituitary gonadotropins to counteract the decrease in estrogen. Therefore, the use of aromatase inhibitors alone in premenopausal women is not a viable treatment option. In postmenopausal women, the ovaries no longer produce estrogen and estrogen is mainly derived from peripheral tissues such as fat, muscle and liver. This process is not regulated by the pituitary gland and androgens are converted to estrogen by the surrounding aromatase enzymes. Because there is no feedback regulation, postmenopausal women do well with aromatase inhibitors. The commonly used aromatase inhibitors are letrozole, anastrozole, and exemestane. Large clinical trials have confirmed that anastrozole is more effective than tamoxifen and has a significantly lower incidence of endometrial cancer and thrombophilia than tamoxifen. The US Breast Cancer Treatment Guidelines state that anastrozole can be used as a direct substitute for tamoxifen in the adjuvant treatment of hormone receptor-positive postmenopausal breast cancer, and that eptifibatide and exemestane can be used at different stages of tamoxifen application.