The DOI matches its Crossref record; 104 of the 105 references it cites were found in a registry or an index.
Circadian Clock, Cancer, and Chemotherapy
Open accessAbstract
The circadian clock is a global regulatory system that interfaces with most other regulatory systems and pathways in mammalian organisms. Investigations of the circadian clock–DNA damage response connections have revealed that nucleotide excision repair, DNA damage checkpoints, and apoptosis are appreciably influenced by the clock. Although several epidemiological studies in humans and a limited number of genetic studies in mouse model systems have indicated that clock disruption may predispose mammals to cancer, well-controlled genetic studies in mice have not supported the commonly held view that circadian clock disruption is a cancer risk factor. In fact, in the appropriate genetic background, clock disruption may instead aid in cancer regression by promoting intrinsic and extrinsic apoptosis. Finally, the clock may affect the efficacy of cancer treatment (chronochemotherapy) by modulating the pharmacokinetics and pharmacodynamics of chemotherapeutic drugs as well as the activity of the DNA repair enzymes that repair the DNA damage caused by anticancer drugs.
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“Circadian misalignment may alter the rhythms of cellular circadian clocks, and it is believed that this may increase the risk of cancer [48].”
From Shift Work: Disrupted Circadian Rhythms and Sleep—Implications for Health and Well-being (2017) · cites this paper as [48]
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Cites
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Self-citationCheckpoints: Controls That Ensure the Order of Cell Cycle Events
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A Serum Shock Induces Circadian Gene Expression in Mammalian Tissue Culture Cells
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Mechanism of Eukaryotic Homologous Recombination
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Transcriptional architecture of the mammalian circadian clock
Takahashi, J. S. (2016) · Nature Reviews Genetics · doi:10.1038/nrg.2016.150 · Cited by 2,786
Shift Work: Disrupted Circadian Rhythms and Sleep—Implications for Health and Well-being
James, S. M., Honn, K. A., Gaddameedhi, S., & Van Dongen, H. P. A. (2017) · Current Sleep Medicine Reports · doi:10.1007/s40675-017-0071-6 · Cited by 517
Self-citationBallesta, A., Innominato, P. F., Dallmann, R., Rand, D. A. J., & Lévi, F. (2017) · Pharmacological Reviews · doi:10.1124/pr.116.013441 · Cited by 348
Clocks, cancer, and chronochemotherapy
Sancar, A., & Gelder, R. N. V. (2020) · Science · doi:10.1126/science.abb0738 · Cited by 285
Self-citationMechanisms of DNA Repair by Photolyase and Excision Nuclease (Nobel Lecture)
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Metadata
- Authors
- Sancar, A., Lindsey-Boltz, L. A., Gaddameedhi, S., Selby, C. P., Ye, R., Chiou, Y.-Y., Kemp, M. G., Hu, J., Lee, J. H., & Ozturk, N.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- University of North Carolina School of Medicine , , , ,
- Corresponding author
- Sancar, Aziz
- ORCID
- Venue
- Biochemistry
- Publisher
- American Chemical Society (ACS)
- Published
- 2014-10-10
- Volume
- 54
- Issue
- 2
- Pages
- 110-123
- ISSN
- 0006-2960 (ISSN-L)
- 1520-4995
- PMC
- PMC4303322
- OpenAlex
- W2139669192
- Cited by
- 170
- References
- 105
- Citations by year
- 2026: 8 · 2025: 15 · 2024: 11 · 2023: 8 · 2022: 14 · 2021: 15 · 2020: 18 · 2019: 18 · 2018: 19 · 2017: 17 · 2016: 18 · 2015: 7 · 2014: 1
- FWCI
- 6.99
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Biochemistry (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institute of General Medical Sciences (GM31082, GM32833)
- National Science Council Taiwan (NA)
- Academia Sinica (NA)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Circular RNAs in diseases
- Keywords
- circadian clock, cancer, DNA damage response, nucleotide excision repair, DNA damage checkpoint, apoptosis, cancer risk, tumor regression, pharmacokinetics, pharmacodynamics, anticancer agents, DNA repair enzymes
- MeSH terms
- Animals, Antineoplastic Agents, DNA Damage, DNA Repair, Humans, Neoplasms, Risk Factors, Apoptosis, DNA Repair Enzymes, Drug Chronotherapy, Circadian Clocks
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