Evidence map›Paper›PMID 37405534›Full record

ReviewMolecular and cellular biochemistry2024

The circadian clock as a potential biomarker and therapeutic target in pancreatic cancer.

Ghazaleh Pourali, Amir Mahmoud Ahmadzade, Mahshid Arastonejad, Roozbeh Pourali, Danial Kazemi, Hamidreza Ghasemirad, Majid Khazaei, Hamid Fiuji, Mohammadreza Nassiri, Seyed Mahdi Hassanian and 2 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Circadian rhythm disruption and endocrine-related tumors.World journal of clinical oncology · 2024
    Review
  8. Review
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

12 authors.

Ghazaleh Pourali *Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Amir Mahmoud Ahmadzade *Transplant Research Center, Clinical Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Mahshid Arastonejad *Department of Human and Molecular Genetics, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA.
Roozbeh Pourali *Student Research Committee, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran.
Danial KazemiStudent Research Committee, Isfahan University of Medical Sciences, Hezar Jerib Street, Isfahan, Iran.
Hamidreza GhasemiradStudent Research Committee, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Majid KhazaeiMetabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Hamid FiujiMetabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohammadreza NassiriBasic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Seyed Mahdi HassanianMetabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Gordon A FernsDivision of Medical Education, Brighton & Sussex Medical School, Falmer, Brighton, Sussex, BN1 9PH, UK.
Amir AvanMetabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. amir.avan1@protonmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PC) has a very high mortality rate globally. Despite ongoing efforts, its prognosis has not improved significantly over the last two decades. Thus, further approaches for optimizing treatment are required. Various biological processes oscillate in a circadian rhythm and are regulated by an endogenous clock. The machinery controlling the circadian cycle is tightly coupled with the cell cycle and can interact with tumor suppressor genes/oncogenes; and can therefore potentially influence cancer progression. Understanding the detailed interactions may lead to the discovery of prognostic and diagnostic biomarkers and new potential targets for treatment. Here, we explain how the circadian system relates to the cell cycle, cancer, and tumor suppressor genes/oncogenes. Furthermore, we propose that circadian clock genes may be potential biomarkers for some cancers and review the current advances in the treatment of PC by targeting the circadian clock. Despite efforts to diagnose pancreatic cancer early, it still remains a cancer with poor prognosis and high mortality rates. While studies have shown the role of molecular clock disruption in tumor initiation, development, and therapy resistance, the role of circadian genes in pancreatic cancer pathogenesis is not yet fully understood and further studies are required to better understand the potential of circadian genes as biomarkers and therapeutic targets.

Indexed as

Biomarkers, TumorCircadian ClocksPancreatic NeoplasmsAnimalsHumansBiomarkers, TumorBiomarkerCircadian clockDiagnosisPancreatic cancerPrognosisTreatment

Identifiers

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Registered trials

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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.