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.
Dr. Russel J. Reiter is Professor of Cell Biology in the Department of Cell Systems and Anatomy at the UT Health, San Antonio, Texas, USA, In addition to his Ph.D. degree, Dr. Reiter has received three honorary M.D. degrees and one honorary D.Sc. degree from international universities. His research relates to the multiple receptor-independent and receptor-dependent actions of melatonin in humans, animals and plants. He has trained 25 Ph.D. students and 144 postdoctoral fellows. Dr. Reiter has received numerous awards for his research including the A. Ross McIntyre Gold Metal (USA), US Senior Scientist Award (Germany), Lizoni Lincee Award (Italy), Inaugural Aaron B. Lerner Pioneer Award (USA), Chulabhorn Royal Academy Medal (Thailand), etc. He has published numerous research papers, reviews and chapters and he has written or edited 25 books. Based on Google Scholar, his papers have been cited in the scientific literature more than 130,000 times and his h-index is 175. Thomson Reuters/ Clarivate Analytics have identified Dr. Reiter as a Highly Cited Scientist (top 1%) and listed him as one of the World’s Most Influential Scientific Minds in 2014. Dr. Reiter has been an invited speaker at more than 300 international meetings and symposia. He is the Co-Editor of Melatonin Research and he is the Founder and past Editor of the Journal of Pineal Research.