Evidence map›Paper›PMID 28420185›Full record

ReviewInternational journal of molecular sciences2017

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis.

Russel J Reiter, Sergio A Rosales-Corral, Dun-Xian Tan, Dario Acuna-Castroviejo, Lilan Qin, Shun-Fa Yang, Kexin Xu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 5 pooled it
20.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

221 citing papers in PubMed, 5 syntheses or guidelines pooled it, 418 citations in OpenAlex.

  1. Influence of melatonin supplementation on cancer-related fatigue: a meta-analysis of randomized controlled trials.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

161 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Russel J ReiterDepartment of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. reiter@uthscsa.edu.
Sergio A Rosales-CorralCentro de Investigacion Biomedica de Occidente, Del Instituto Mexicano del Seguro Social, Guadalajara 44340, Mexico. espiral17@gmail.com.
Dun-Xian TanDepartment of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. tan@uthscsa.edu.
Dario Acuna-CastroviejoCentro de Investigacion Biomedica, Universidad de Granada, Granada 18916, Spain. dacuna@ugr.es.
Lilan QinDepartment of Cell Systems and Anatomy, UT Health, San Antonio, TX 78229, USA. qinlilan1980@gmail.com.
Shun-Fa YangInstitute of Medicine, Chung Shan, Medical University, Taichung 40201, Taiwan. ysf@csmu.edu.tw.
Kexin XuDepartment of Molecular Medicine, UT Health, San Antonio, TX 78229, USA. xuk3@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · USChung Shan Medical University · TWMexican Social Security Institute · MXUniversidad de Granada · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCell Transformation, NeoplasticDisease ProgressionDNA DamageDrug Resistance, NeoplasmGenomic InstabilityHumansMelatoninNeoplasm MetastasisNeoplasmsRadiation-Protective AgentsTreatment OutcomeAntineoplastic AgentsMelatoninRadiation-Protective Agentsangiogenesisantioxidantapoptosisbreastchemotherapyfree radicalsinvasionionizing radiationmelatonin receptorsmolecular mechanismsprostate

Identifiers

PMID28420185
PMCPMC5412427
OpenAlexW2606778500

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.