I. History of the development of endocrine therapy for breast cancer Endocrine therapy for breast cancer has a history of more than 100 years. Firstly, in 1895, Dr. Geoage Thomas Beaston of Glasgow Oncology Hospital in the UK achieved good therapeutic results in treating recurrent metastatic breast cancer with bilateral oophorectomy, and the description of his condition was published in Lancet in 1896, which was a sensation and became the beginning of endocrine treatment of breast cancer. The presentation was published in the Lancet in 1896 and became a sensation, becoming the beginning of research and development of endocrine therapy for breast cancer. The Glasgow Cancer Hospital also eventually named its hospital after Beaston, and the Beaston Cancer Center is now the most prestigious cancer hospital in Europe. The second event was the successful isolation of the estrogen receptor from breast cancer cells and the advancement of its molecular biology, which led to the development of endocrine-targeted molecular therapy. The third event was the gradual introduction of third-generation aromatase inhibitors (AIs) by the 1990s. A series of clinical studies established the effectiveness of third-generation AIs in endocrine therapy, making them another first-line drug for endocrine treatment of breast cancer after TAM. Other important events in the development of breast cancer endocrine therapy are listed in the table below. From this table, we can see that as the mechanism of breast cancer endocrine therapy is gradually understood, endocrine therapy for breast cancer is becoming more and more targeted, invasive endocrine therapy is gradually replaced by drug therapy, and the side effects of drugs are relatively less and less. The whole history of endocrine therapy for breast cancer is the transition from surgical endocrine adenomectomy to the development of endocrine therapeutic drugs. The basic concept of endocrine therapy for breast cancer is mainly applied to patients with hormone-dependent breast cancer, i.e. breast cancer that responds to estrogen and progesterone stimulation, i.e. patients with estrogen receptor (ER) or progesterone receptor (PR) positive, while endocrine therapy is not effective for non-hormone-dependent breast cancer. 2. The main mechanism of endocrine therapy is to inhibit the growth of hormone-dependent tumor cells by reducing estrogen levels or inhibiting estrogen action in the body; 3. Even if only stable disease (SD) is achieved, the survival time of patients can be significantly prolonged; 5.After one endocrine therapy is effective and the treatment fails, the change to other endocrine therapy may still be effective and there is a chance to switch to chemotherapy; 6.Because of the small side effects, endocrine therapy for breast cancer can be maintained for a long time, the treatment is well tolerated and patients have a high quality of life; 7.The older the age and the longer the time of menopause, the better the effect of endocrine therapy. the older the age, the longer the time of menopause, the better the effect of endocrine therapy; 8. The main therapeutic drugs of endocrine therapy are listed below: Figure 2: Main drugs of endocrine therapy 9. The main endocrine therapeutic drugs used in clinical practice are still mainly TAM and third generation AIs. their mechanism of action is shown below. TAM (SERM class of drugs) mainly inhibits the stimulating effect of estrogen on breast cancer AIs (exemestane, letrozole, etc., which are commonly used in clinical practice) are used to inhibit the effect of aromatase in peripheral tissues of menopausal patients thereby reducing the conversion of androgens into estrogens in patients and achieving the effect of lowering estrogen levels in patients’ bodies to suppress tumors. Therefore, AIs can only be used in menopausal breast cancer patients.