Hormones Introduction Sex hormones are closely related to the occurrence and development of some common malignant tumors in humans, such as breast cancer and endometrial cancer in women, and prostate cancer in men. Initially, in 1896, a man named Beaston found that tumors shrank after removal of ovaries in breast cancer patients, and in 1941, Huggings found that tumors regressed after removal of testes in prostate cancer patients, thus finding a correlation between hormone levels and tumors. Similarly, pathophysiological studies have confirmed that human hormones, such as some growth factors, stimulate the growth and differentiation of epithelial cells in tissues. If the growth and differentiation is excessive, it increases the risk of tumor development, for example, some tissues and organs will not develop tumors if they are not stimulated by hormones. For example, men who remove their testicles do not develop prostate cancer. For hormone-dependent tissues and organs, sex hormones are necessary for their growth and maintenance of cellular activity. Breast cancer Breast cancer epidemiology in relation to hormones Breast cancer is age-specific as well as regionally variable; for example, the incidence of breast cancer is significantly higher in women in Western countries than in non-Western countries. For example, the incidence of breast cancer in women in Western countries is significantly higher than in non-Western countries, and the incidence of breast cancer in women in countries where economic conditions are becoming better and diets are changing is also significantly higher. Current epidemiological studies have confirmed that some changes in the female reproductive system can become a risk factor for breast cancer, for example: 1. For the occurrence of female breast cancer, the risk factors include: early age of menarche, late birth of the first child, reduction in the number of births, and delayed age of menopause. All these risk factors are closely related to the influence of female hormones, especially estrogen. 2. The decrease in the incidence of breast cancer is related to surgically induced menopause, for example, the removal of ovaries causes menopause, thus reducing the incidence of breast cancer. In addition, for postmenopausal women, if the endogenous estrogen is elevated or the exogenous estrogen is elevated due to medication, the incidence of breast cancer will increase. It is currently believed that hormone replacement therapy increases the incidence of breast cancer in women with tumors that are primarily estrogen receptor positive and sensitive to hormone replacement therapy. In addition, for women over the age of 65, estrogen replacement therapy alone does not increase the incidence of breast cancer, but estrogen and luteinizing hormone together increase the incidence of breast cancer. Therefore, sex hormones can only partially explain the occurrence of breast cancer. In addition individual differences, i.e., individual weight and height, play a very important role in the geographic incidence of breast cancer. It has been found that for women who immigrated from non-Western countries to Western countries, their breast cancer incidence is basically attributed to many non-genetic factors, such as: 1. For Asian women who are second and third generation immigrants to the United States, their breast cancer incidence tends to increase gradually compared to native women. This is due to changes in lifestyle during adolescence or after immigration in late adulthood, lack of exercise, or late childbearing due to the liberalization of Western women. 2. Another epidemiological study found that the early timing of a woman’s first pregnancy is beneficial as it allows for complete differentiation of the breast tissue. Generally, the longer the time from breast development and proliferation to complete differentiation of breast in women, the more likely this time increases the susceptibility to breast cancer and the risk of developing the disease. Therefore, the risk factors of breast cancer are closely related to the length of this time, i.e., to the length of time from the proliferation period of the breast epithelial cells in women’s puberty to the complete differentiation of the breast caused by pregnancy. Prevention and treatment of breast cancer Because a large number of breast cancer patients are hormone-dependent, our concept of prevention and treatment of breast is the application of estrogen antagonists or inhibition of estrogen synthesis. 1. Because it is now known how estrogen is produced in the body, humans have developed many estrogen antagonists, such as tamoxifen, or raloxifene. Some of the larger clinical trials have confirmed that preventive use of estrogen antagonists (tamoxifen or raloxifene) in women at high risk for breast cancer results in a lower incidence of estrogen receptor-positive (ER+) breast cancer. In addition, clinical trials have also demonstrated that postmenopausal women with aromatase inhibitors can reduce estrogen production, which also reduces the incidence of breast cancer, but they have not been used for large-scale prevention in high-risk groups. 2. There are no clinical trials to confirm that the use of pregnancy-related hormones makes the female mammary gland fully differentiated and mature, while animal studies can use human chorionic gonadotropin (hCG). However, this is likely to complicate the situation because in humans, the mammary gland only fully differentiates and matures during a complete pregnancy cycle, thus preventing breast cancer, whereas in the intervening period, if a spontaneous or artificial abortion occurs and the pregnancy is interrupted, breast cancer prevention will not be achieved. Human chorionic gonadotropin (hCG) is released most during the first month of pregnancy. 3. To date, all methods using changes in a woman’s nutritional diet have not been successful in reducing the risk of breast cancer. Perhaps in the near future, scientists will be able to identify which groups of people will benefit from specific dietary habits from more detailed population subgroups. Endometrial Cancer Endometrial cancer is currently the most common gynecologic tumor in menopausal women. The incidence of endometrial cancer varies worldwide, with the highest incidence in Picasso. Risk factors for endometrial cancer, such as early age of menarche, postponed age of menopause, and women without childbirth, as well as some factors directly related to elevated estrogen content, such as obesity or polycystic ovary syndrome, etc.: 1. Women with body mass index (BMI) >30 have 3 times the risk of endometrial cancer as women with BMI <25. 2. Overweight >20 kg in adult women significantly increases the risk of endometrial cancer. 3. Diabetes and hypertension also increase the risk of endometrial cancer, while smoking, low-fat diet and exercise reduce the risk of endometrial cancer. The reason for this is likely to indirectly affect the level of estrogen in the body. At present, experts believe that obesity is closely related to type I endometrial cancer, which is estrogen-dependent, and this type accounts for 80% of the endometrial cancer population. For postmenopausal women, long-term use of estrogen replacement therapy significantly increases the risk of endometrial cancer, but if estrogen replacement therapy is combined with progestin therapy, the risk of endometrial cancer does not increase because progestin protects the endometrium. Currently, progestins can be administered vaginally or directly through the endometrial route. In addition, there is another protective option that is considered promising, which is a tiny device that can be placed in the uterus that releases progestin periodically and for many years. Prostate Cancer Epidemiology and Hormone Relationships Current epidemiology has demonstrated a strong relationship between prostate cancer and environmental factors, particularly dietary and nutritional health, as well as lifestyle and genetic inheritance. The incidence and mortality of prostate cancer increases with age. Genetic prostate cancer susceptibility genes have now been found to be associated with the development of inflammation, which suggests that infection and inflammation can lead to the early development of prostate tumors. Prostate cancer prevention Current clinical trials for prostate cancer chemoprevention use a substance called finasteride, which is chemically a 5-alpha-reductase inhibitor that converts androgens to dihydrotestosterone (DHT). Finasteride has now been shown to block or delay the expression of prostate-specific antigen (PSA) in the plasma of prostate cancer patients to <3 ng/ml. Conclusion Tumor prevention can currently be achieved through the control of hormone levels in the body, which remains an interesting line of research. In the field of breast cancer, doctors have achieved good and positive preventive effects by using drugs in high-risk groups to interfere with the biosynthesis of estrogen and affect its metabolism. In contrast, there are fewer similar clinical trials for endometrial and prostate cancers. Because of the lack of specific hormonal control and interference with dietary levels, prevention studies for these two diseases are still in progress.