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Summary. Radiation therapy (RT) plays a key role in the treatment of malignant tumor diseases in the majority of cancer patients. Unfortunately, despite the improvement of RT methods and tools (in particular, its conformal strategy) and modern methods of dosimetry, RT has a harmful effect not only on the tumor, but also on normal tissues surrounding the tumor. In some cases, this leads to the development of radiation reactions and complications, the treatment of which is a long, sometimes ineffective process. One of the strategies to prevent or reduce these complications is the use of natural radioprotectors, among which the pineal hormone melatonin deserves attention. It is a powerful antioxidant with immunoregulatory properties that can reduce toxicity caused by ionizing radiation (IR) in various organs. These effects are mediated by the modulatory effects of melatonin at different levels of tissue response to IR. The most important are the effects on the DNA repair system, antioxidant enzymes, immune cells, cytokine secretion, transcription factors and protein kinases. The data highlighted in this review indicate that melatonin has great potential to prevent the side effects of RT and its inclusion as an adjuvant in RT would enable the use of higher radiation doses in treatment. In addition, due to the antitumor and radiosensitizing properties of melatonin, its use can increase tumor damage. Therefore, melatonin is a promising radioprotective agent of normal tissues surrounding the tumor with the effect of increasing the therapeutic efficiency/toxicity ratio of chemoradiation treatment of patients.
Summary. Radiation therapy (RT) plays a key role in the treatment of malignant tumor diseases in the majority of cancer patients. Unfortunately, despite the improvement of RT methods and tools (in particular, its conformal strategy) and modern methods of dosimetry, RT has a harmful effect not only on the tumor, but also on normal tissues surrounding the tumor. In some cases, this leads to the development of radiation reactions and complications, the treatment of which is a long, sometimes ineffective process. One of the strategies to prevent or reduce these complications is the use of natural radioprotectors, among which the pineal hormone melatonin deserves attention. It is a powerful antioxidant with immunoregulatory properties that can reduce toxicity caused by ionizing radiation (IR) in various organs. These effects are mediated by the modulatory effects of melatonin at different levels of tissue response to IR. The most important are the effects on the DNA repair system, antioxidant enzymes, immune cells, cytokine secretion, transcription factors and protein kinases. The data highlighted in this review indicate that melatonin has great potential to prevent the side effects of RT and its inclusion as an adjuvant in RT would enable the use of higher radiation doses in treatment. In addition, due to the antitumor and radiosensitizing properties of melatonin, its use can increase tumor damage. Therefore, melatonin is a promising radioprotective agent of normal tissues surrounding the tumor with the effect of increasing the therapeutic efficiency/toxicity ratio of chemoradiation treatment of patients.
Cancer is a large group of diseases and the second leading cause of death worldwide. Lung, prostate, colorectal, stomach, and liver cancers are the most common types of cancer in men, whereas breast, colorectal, lung, cervical, and thyroid cancers are the most common among women. Presently, various treatment strategies, including surgical resection combined with chemotherapy, radiotherapy, nanotherapy, and immunotherapy, have been used as conventional treatments for patients with cancer. However, the clinical outcomes of advanced-stage disease remain relatively unfavorable owing to the emergence of chemoresistance, toxicity, and other undesired detrimental side effects. Therefore, new therapies to overcome these limitations are indispensable. Recently, there has been considerable evidence from experimental and clinical studies suggesting that melatonin can be used to prevent and treat cancer. Studies have confirmed that melatonin mitigates the pathogenesis of cancer by directly affecting carcinogenesis and indirectly disrupting the circadian cycle. Melatonin (MLT) is nontoxic and exhibits a range of beneficial effects against cancer via apoptotic, antiangiogenic, antiproliferative, and metastasis-inhibitory pathways. The combination of melatonin with conventional drugs improves the drug sensitivity of cancers, including solid and liquid tumors. In this manuscript, we will comprehensively review some of the cellular, animal, and human studies from the literature that provide evidence that melatonin has oncostatic and anticancer properties. Further, this comprehensive review compiles the available experimental and clinical data analyzing the history, epidemiology, risk factors, therapeutic effect, clinical significance, of melatonin alone or in combination with chemotherapeutic agents or radiotherapy, as well as the underlying molecular mechanisms of its anticancer effect against lung, breast, prostate, colorectal, skin, liver, cervical, and ovarian cancers. Nonetheless, in the interest of readership clarity and ease of reading, we have discussed the overall mechanism of the anticancer activity of melatonin against different types of cancer. We have ended this report with general conclusions and future perspectives.
Fibrosis and pneumonitis are the most important side effects of lung tissue following cancer therapy. Radiotherapy and chemotherapy by some drugs such as bleomycin can induce pneumonitis and fibrosis. Targeted therapy and immunotherapy also may induce pneumonitis and fibrosis with a lesser extent compared to chemotherapy and radiotherapy. Activation of lymphocytes by immunotherapy or infiltration of inflammatory cells such as macrophages, lymphocytes, neutrophils, and mast cells following chemo/radiation therapy can induce pneumonitis. Furthermore, the polarization of macrophages toward M2 cells and the release of anti-inflammatory cytokines stimulate fibrosis. Lung fibrosis and pneumonitis may also be potentiated by some other changes such as epithelial-mesenchymal transition (EMT), oxidative stress, reduction/oxidation (redox) responses, renin-angiotensin system, and the upregulation of some inflammatory mediators such as nuclear factor of kappa B (NF-κB), inflammasome, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Damages to the lung vascular system and the induction of hypoxia also can induce pulmonary injury following chemo/radiation therapy. In this review, we explain various mechanisms of the induction of pneumonitis and lung fibrosis following cancer therapy. Furthermore, the targets and promising agents to mitigate lung fibrosis and pneumonitis will be discussed.
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