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 cellular circadian clock rhythms and is believed to increase cancer risk.
“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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Redox clocks: Time to rethink redox interventions
Nagy, A. D., & Reddy, A. B. (2017) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2017.12.033 · Cited by 12 · see citing works
Moleculer nutritional immunology and cancer
Çehreli, R. (2018) · Journal of Oncological Sciences · doi:10.1016/j.jons.2018.02.002 · Cited by 11 · see citing works
The circadian clock, aging and its implications in cancer
Rezaeian, A.-H., Dang, F., & Wei, W. (2023) · Neoplasia · doi:10.1016/j.neo.2023.100904 · Cited by 10 · see citing works
Architecture and mechanism of the central gear in an ancient molecular timer
Egli, M. (2017) · Journal of The Royal Society Interface · doi:10.1098/rsif.2016.1065 · Cited by 10 · see citing works
Mechanismen der DNA‐Reparatur durch Photolyasen und Exzisionsnukleasen (Nobel‐Aufsatz)
Sancar, A. (2016) · Angewandte Chemie · doi:10.1002/ange.201601524 · Cited by 10 · see citing works
Self-citation
- 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 · 2013: 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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