New paper below.
See also my post of 6 months back:
There seems to be a lack of interest in melatonin. I take 50 mg every night & am dissapointed in the paucity of papers. Here's an understatement from the new paper:
"Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level."
Int J Mol Sci. 2017 Apr 17;18(4). pii: E843. doi: 10.3390/ijms18040843.
Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis.
Reiter RJ1, Rosales-Corral SA2, Tan DX3, Acuna-Castroviejo D4, Qin L5, Yang SF6, Xu K7.
Department of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. email@example.com.
Centro de Investigacion Biomedica de Occidente, Del Instituto Mexicano del Seguro Social, Guadalajara 44340, Mexico. firstname.lastname@example.org.
Department of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. email@example.com.
Centro de Investigacion Biomedica, Universidad de Granada, Granada 18916, Spain. firstname.lastname@example.org.
Department of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. email@example.com.
Institute of Medicine, Chung Shan, Medical University, Taichung 40201, Taiwan. firstname.lastname@example.org.
Department of Molecular Medicine, UT Health, San Antonio, TX 78229, USA. email@example.com.
There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin's co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.
angiogenesis; antioxidant; apoptosis; breast; chemotherapy; free radicals; invasion; ionizing radiation; melatonin receptors; molecular mechanisms; prostate
PMID: 28420185 DOI: 10.3390/ijms18040843