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In vitro studies by Vijayalaxmi et al. (1995) found that melatonin had a significant protective effect on the chromosomal damage of human peripheral lymphocytes caused by γ-rays (150cGy) of 137Cs, and showed a dose-response relationship; physical and chemical effects on free radicals Mutagenicity and carcinogenicity are antagonistic. In vitro experiments have shown that melatonin also has a protective effect on the mutagenicity caused by self-immobilization C. Melatonin reduces the formation of DNA adducts induced by chemical carcinogens (safrole) and prevents DNA damage. Jianjun Yan et al. studied the anti-tumor effect of melatonin on H22 liver cancer mice, and found that it can inhibit the tumor growth and prolong the survival time of tumor-bearing mice, and has obvious synergy with IL-2. Danforth et al measured the 24-hour plasma melatonin levels of women in normal, breast cancer, and breast cancer-prone patients, respectively, and found that normal women had a circadian rhythm; the circadian rhythm of breast cancer patients was significantly related to the amount of steroid receptors in the primary tumor related. In patients with positive estrogen (ER) or progesterone (PR) receptors, the mean day-to-night plasma melatonin level was significantly lower than that in patients with ER or PR negative tumors, and was significantly negatively correlated with the amount of ER or PR receptors in the primary tumor , indicating that melatonin has a certain correlation with hormone-dependent human breast cancer. Melatonin promotes endogenous granulocyte/macrophage-promoting accumulation factor production by myeloid T-cells and can be used as an adjuvant therapy for tumors.