Evidence map›Paper›PMID 33638890›Full record

ArticleJournal of pineal research2021

Night shift schedule causes circadian dysregulation of DNA repair genes and elevated DNA damage in humans.

Bala S C Koritala, Kenneth I Porter, Osama A Arshad, Rajendra P Gajula, Hugh D Mitchell, Tarana Arman, Mugimane G Manjanatha, Justin Teeguarden, Hans P A Van Dongen, Jason E McDermott and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of pineal research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 93 citations in OpenAlex.

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  9. Circadian clock and cancer.Military Medical Research · 2026
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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

11 authors at 6 institutions in 1 country.

Bala S C KoritalaDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA.ORCID https://orcid.org/0000-0003-4457-093X
Kenneth I PorterDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA.ORCID https://orcid.org/0000-0003-3644-1011
Osama A ArshadComputational Biology and Bioinformatics, Pacific Northwest National Laboratory, Richland, WA, USA.
Rajendra P GajulaDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA.ORCID http://orcid.org/0000-0002-3446-8555
Hugh D MitchellComputational Biology and Bioinformatics, Pacific Northwest National Laboratory, Richland, WA, USA.ORCID https://orcid.org/0000-0003-0143-8461
Tarana ArmanDepartment of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA.ORCID https://orcid.org/0000-0001-7078-5884
Mugimane G ManjanathaDivision of Genetic and Molecular Toxicology, National Center for Toxicology Research, US Food and Drug Administration, Jefferson, AR, USA.ORCID https://orcid.org/0000-0001-6296-6271
Justin TeeguardenBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA.ORCID https://orcid.org/0000-0003-3817-4391
Hans P A Van DongenSleep and Performance Research Center, Washington State University, Spokane, WA, USA.ORCID https://orcid.org/0000-0002-4678-2971
Jason E McDermottComputational Biology and Bioinformatics, Pacific Northwest National Laboratory, Richland, WA, USA.ORCID https://orcid.org/0000-0003-2961-2572
Shobhan GaddameedhiDepartment of Biological Sciences and Toxicology Program, North Carolina State University, Raleigh, NC, USA.ORCID https://orcid.org/0000-0002-4978-6951
Washington State University Spokane · USPacific Northwest National Laboratory · USCincinnati Children's Hospital Medical Center · USNational Center for Toxicological Research · USNorth Carolina State University · USOregon State University · US

Funding

Translational Research Support CoreP30ES025128 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Kelly Sides · 2015 to 2026
$18.3M
DNA Repair Mechanisms and Circadian Clock Disruption in the CorneaR01ES030113 · NIEHS · WASHINGTON STATE UNIVERSITY · PI GADDAMEEDHI, SHOBHAN · 2020 to 2025
$2.1M
Chronotherapy as a Strategy to Attenuate Toxicity Associated with Cisplatin and Radiation Treatment for Triple-Negative Breast CancerR21CA227381 · NCI · WASHINGTON STATE UNIVERSITY · PI GADDAMEEDHI, SHOBHAN · 2018 to 2019
$361k
Battelle for the US Department of Energy DE-AC05-76RL01830BRAVECDMRP Peer Reviewed Cancer Research Program CA171123NCI NIH HHS L30 CA171123NCI NIH HHS R21 CA227381NIEHS NIH HHS P30 ES025128NIEHS NIH HHS R01 ES030113NIH HHS R01ES030113NIH HHS R21CA227381North Carolina State University P30ES025128United States Army Medical Research and Development Command W81XWH-18-1-0100Washington State University
6 · The paper itself

Abstract

Circadian disruption has been identified as a risk factor for health disorders such as obesity, cardiovascular disease, and cancer. Although epidemiological studies suggest an increased risk of various cancers associated with circadian misalignment due to night shift work, the underlying mechanisms have yet to be elucidated. We sought to investigate the potential mechanistic role that circadian disruption of cancer hallmark pathway genes may play in the increased cancer risk in shift workers. In a controlled laboratory study, we investigated the circadian transcriptome of cancer hallmark pathway genes and associated biological pathways in circulating leukocytes obtained from healthy young adults during a 24-hour constant routine protocol following 3 days of simulated day shift or night shift. The simulated night shift schedule significantly altered the normal circadian rhythmicity of genes involved in cancer hallmark pathways. A DNA repair pathway showed significant enrichment of rhythmic genes following the simulated day shift schedule, but not following the simulated night shift schedule. In functional assessments, we demonstrated that there was an increased sensitivity to both endogenous and exogenous sources of DNA damage after exposure to simulated night shift. Our results suggest that circadian dysregulation of DNA repair may increase DNA damage and potentiate elevated cancer risk in night shift workers.

Indexed as

Circadian RhythmDNA DamageDNA RepairTranscriptomeActivity CyclesAdultBiomarkers, TumorChronobiology DisordersFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleNeoplasmsRisk AssessmentRisk FactorsBiomarkers, Tumorcircadian misalignmentgenomic stabilityhallmarks of cancershift work

Identifiers

PMID33638890
PMCPMC8011353
OpenAlexW3132046378

What OpenQuestion holds

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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.