Circadian clock, cancer, and chemotherapy
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Sancar, A. | - |
dc.contributor.author | Lindsey-Boltz, L.A. | - |
dc.contributor.author | Gaddameedhi, S. | - |
dc.contributor.author | Selby, C.P. | - |
dc.contributor.author | Ye, R. | - |
dc.contributor.author | Chiou, Y.-Y. | - |
dc.contributor.author | Kemp, M.G. | - |
dc.contributor.author | Hu, J. | - |
dc.contributor.author | Lee, J.H. | - |
dc.contributor.author | Ozturk, N. | - |
dc.date.accessioned | 2021-09-04T23:53:48Z | - |
dc.date.available | 2021-09-04T23:53:48Z | - |
dc.date.created | 2021-06-17 | - |
dc.date.issued | 2015 | - |
dc.identifier.issn | 0006-2960 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/95903 | - |
dc.description.abstract | 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. © 2014 American Chemical Society. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | American Chemical Society | - |
dc.subject | Cell death | - |
dc.subject | Chemotherapy | - |
dc.subject | Diseases | - |
dc.subject | DNA | - |
dc.subject | Genetic engineering | - |
dc.subject | Mammals | - |
dc.subject | Repair | - |
dc.subject | Chemotherapeutic drugs | - |
dc.subject | DNA damage response | - |
dc.subject | DNA-repair enzymes | - |
dc.subject | Epidemiological studies | - |
dc.subject | Genetic backgrounds | - |
dc.subject | Nucleotide excision repair | - |
dc.subject | Pharmacokinetics and pharmacodynamics | - |
dc.subject | Regulatory systems | - |
dc.subject | Clocks | - |
dc.subject | antineoplastic agent | - |
dc.subject | ATR protein | - |
dc.subject | checkpoint kinase 1 | - |
dc.subject | DNA | - |
dc.subject | excision repair cross complementing protein 1 | - |
dc.subject | protein BMAL1 | - |
dc.subject | protein p53 | - |
dc.subject | protein p63 | - |
dc.subject | protein p73 | - |
dc.subject | protein timeless | - |
dc.subject | transcription factor CLOCK | - |
dc.subject | transcription factor IIH | - |
dc.subject | xeroderma pigmentosum group A protein | - |
dc.subject | xeroderma pigmentosum group C protein | - |
dc.subject | antineoplastic agent | - |
dc.subject | DNA ligase | - |
dc.subject | apoptosis | - |
dc.subject | Article | - |
dc.subject | cancer chemotherapy | - |
dc.subject | cancer growth | - |
dc.subject | cancer risk | - |
dc.subject | carcinogenesis | - |
dc.subject | chronotherapy | - |
dc.subject | circadian rhythm | - |
dc.subject | direct DNA repair | - |
dc.subject | disease association | - |
dc.subject | DNA damage | - |
dc.subject | DNA damage checkpoint | - |
dc.subject | DNA repair | - |
dc.subject | DNA replication | - |
dc.subject | enzyme phosphorylation | - |
dc.subject | excision repair | - |
dc.subject | G1 phase cell cycle checkpoint | - |
dc.subject | G2 phase cell cycle checkpoint | - |
dc.subject | gene repression | - |
dc.subject | high risk population | - |
dc.subject | human | - |
dc.subject | M phase cell cycle checkpoint | - |
dc.subject | mismatch repair | - |
dc.subject | neoplasm | - |
dc.subject | nonhuman | - |
dc.subject | priority journal | - |
dc.subject | protein function | - |
dc.subject | recombination repair | - |
dc.subject | shift worker | - |
dc.subject | signal transduction | - |
dc.subject | suprachiasmatic nucleus | - |
dc.subject | ultraviolet radiation | - |
dc.subject | animal | - |
dc.subject | chronopharmacology | - |
dc.subject | DNA repair | - |
dc.subject | drug effects | - |
dc.subject | genetics | - |
dc.subject | metabolism | - |
dc.subject | Neoplasms | - |
dc.subject | risk factor | - |
dc.subject | Mammalia | - |
dc.subject | Mus | - |
dc.subject | Animals | - |
dc.subject | Antineoplastic Agents | - |
dc.subject | Apoptosis | - |
dc.subject | Circadian Clocks | - |
dc.subject | DNA Damage | - |
dc.subject | DNA Repair | - |
dc.subject | DNA Repair Enzymes | - |
dc.subject | Drug Chronotherapy | - |
dc.subject | Humans | - |
dc.subject | Neoplasms | - |
dc.subject | Risk Factors | - |
dc.title | Circadian clock, cancer, and chemotherapy | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, J.H. | - |
dc.identifier.doi | 10.1021/bi5007354 | - |
dc.identifier.scopusid | 2-s2.0-84922448694 | - |
dc.identifier.bibliographicCitation | Biochemistry, v.54, no.2, pp.110 - 123 | - |
dc.relation.isPartOf | Biochemistry | - |
dc.citation.title | Biochemistry | - |
dc.citation.volume | 54 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 110 | - |
dc.citation.endPage | 123 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | Cell death | - |
dc.subject.keywordPlus | Chemotherapy | - |
dc.subject.keywordPlus | Diseases | - |
dc.subject.keywordPlus | DNA | - |
dc.subject.keywordPlus | Genetic engineering | - |
dc.subject.keywordPlus | Mammals | - |
dc.subject.keywordPlus | Repair | - |
dc.subject.keywordPlus | Chemotherapeutic drugs | - |
dc.subject.keywordPlus | DNA damage response | - |
dc.subject.keywordPlus | DNA-repair enzymes | - |
dc.subject.keywordPlus | Epidemiological studies | - |
dc.subject.keywordPlus | Genetic backgrounds | - |
dc.subject.keywordPlus | Nucleotide excision repair | - |
dc.subject.keywordPlus | Pharmacokinetics and pharmacodynamics | - |
dc.subject.keywordPlus | Regulatory systems | - |
dc.subject.keywordPlus | Clocks | - |
dc.subject.keywordPlus | antineoplastic agent | - |
dc.subject.keywordPlus | ATR protein | - |
dc.subject.keywordPlus | checkpoint kinase 1 | - |
dc.subject.keywordPlus | DNA | - |
dc.subject.keywordPlus | excision repair cross complementing protein 1 | - |
dc.subject.keywordPlus | protein BMAL1 | - |
dc.subject.keywordPlus | protein p53 | - |
dc.subject.keywordPlus | protein p63 | - |
dc.subject.keywordPlus | protein p73 | - |
dc.subject.keywordPlus | protein timeless | - |
dc.subject.keywordPlus | transcription factor CLOCK | - |
dc.subject.keywordPlus | transcription factor IIH | - |
dc.subject.keywordPlus | xeroderma pigmentosum group A protein | - |
dc.subject.keywordPlus | xeroderma pigmentosum group C protein | - |
dc.subject.keywordPlus | antineoplastic agent | - |
dc.subject.keywordPlus | DNA ligase | - |
dc.subject.keywordPlus | apoptosis | - |
dc.subject.keywordPlus | Article | - |
dc.subject.keywordPlus | cancer chemotherapy | - |
dc.subject.keywordPlus | cancer growth | - |
dc.subject.keywordPlus | cancer risk | - |
dc.subject.keywordPlus | carcinogenesis | - |
dc.subject.keywordPlus | chronotherapy | - |
dc.subject.keywordPlus | circadian rhythm | - |
dc.subject.keywordPlus | direct DNA repair | - |
dc.subject.keywordPlus | disease association | - |
dc.subject.keywordPlus | DNA damage | - |
dc.subject.keywordPlus | DNA damage checkpoint | - |
dc.subject.keywordPlus | DNA repair | - |
dc.subject.keywordPlus | DNA replication | - |
dc.subject.keywordPlus | enzyme phosphorylation | - |
dc.subject.keywordPlus | excision repair | - |
dc.subject.keywordPlus | G1 phase cell cycle checkpoint | - |
dc.subject.keywordPlus | G2 phase cell cycle checkpoint | - |
dc.subject.keywordPlus | gene repression | - |
dc.subject.keywordPlus | high risk population | - |
dc.subject.keywordPlus | human | - |
dc.subject.keywordPlus | M phase cell cycle checkpoint | - |
dc.subject.keywordPlus | mismatch repair | - |
dc.subject.keywordPlus | neoplasm | - |
dc.subject.keywordPlus | nonhuman | - |
dc.subject.keywordPlus | priority journal | - |
dc.subject.keywordPlus | protein function | - |
dc.subject.keywordPlus | recombination repair | - |
dc.subject.keywordPlus | shift worker | - |
dc.subject.keywordPlus | signal transduction | - |
dc.subject.keywordPlus | suprachiasmatic nucleus | - |
dc.subject.keywordPlus | ultraviolet radiation | - |
dc.subject.keywordPlus | animal | - |
dc.subject.keywordPlus | chronopharmacology | - |
dc.subject.keywordPlus | DNA repair | - |
dc.subject.keywordPlus | drug effects | - |
dc.subject.keywordPlus | genetics | - |
dc.subject.keywordPlus | metabolism | - |
dc.subject.keywordPlus | Neoplasms | - |
dc.subject.keywordPlus | risk factor | - |
dc.subject.keywordPlus | Mammalia | - |
dc.subject.keywordPlus | Mus | - |
dc.subject.keywordPlus | Animals | - |
dc.subject.keywordPlus | Antineoplastic Agents | - |
dc.subject.keywordPlus | Apoptosis | - |
dc.subject.keywordPlus | Circadian Clocks | - |
dc.subject.keywordPlus | DNA Damage | - |
dc.subject.keywordPlus | DNA Repair | - |
dc.subject.keywordPlus | DNA Repair Enzymes | - |
dc.subject.keywordPlus | Drug Chronotherapy | - |
dc.subject.keywordPlus | Humans | - |
dc.subject.keywordPlus | Neoplasms | - |
dc.subject.keywordPlus | Risk Factors | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.