Redox proteins and radiotherapy.
Identifieur interne : 000619 ( Main/Exploration ); précédent : 000618; suivant : 000620Redox proteins and radiotherapy.
Auteurs : Y. Zhang [Royaume-Uni] ; S G Martin [Royaume-Uni]Source :
- Clinical oncology (Royal College of Radiologists (Great Britain)) [ 1433-2981 ] ; 2014.
Descripteurs français
- KwdFr :
- Antioxydants (métabolisme), Compléments alimentaires (MeSH), Espèces réactives de l'oxygène (métabolisme), Glutarédoxines (métabolisme), Glutathion (métabolisme), Homéostasie (effets des médicaments et des substances chimiques), Humains (MeSH), Oxydoréduction (MeSH), Peroxirédoxines (métabolisme), Pronostic (MeSH), Radicaux libres (métabolisme), Radiosensibilisants (pharmacologie), Radiotolérance (physiologie), Superoxide dismutase (métabolisme), Thiorédoxines (métabolisme), Transduction du signal (MeSH), Tumeurs (diagnostic), Tumeurs (métabolisme), Tumeurs (radiothérapie), Tumeurs (traitement médicamenteux).
- MESH :
- diagnostic : Tumeurs.
- effets des médicaments et des substances chimiques : Homéostasie.
- métabolisme : Antioxydants, Espèces réactives de l'oxygène, Glutarédoxines, Glutathion, Peroxirédoxines, Radicaux libres, Superoxide dismutase, Thiorédoxines, Tumeurs.
- pharmacologie : Radiosensibilisants.
- physiologie : Radiotolérance.
- radiothérapie : Tumeurs.
- traitement médicamenteux : Tumeurs.
- Compléments alimentaires, Humains, Oxydoréduction, Pronostic, Transduction du signal.
English descriptors
- KwdEn :
- Antioxidants (metabolism), Dietary Supplements (MeSH), Free Radicals (metabolism), Glutaredoxins (metabolism), Glutathione (metabolism), Homeostasis (drug effects), Humans (MeSH), Neoplasms (diagnosis), Neoplasms (drug therapy), Neoplasms (metabolism), Neoplasms (radiotherapy), Oxidation-Reduction (MeSH), Peroxiredoxins (metabolism), Prognosis (MeSH), Radiation Tolerance (physiology), Radiation-Sensitizing Agents (pharmacology), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH), Superoxide Dismutase (metabolism), Thioredoxins (metabolism).
- MESH :
- chemical , metabolism : Antioxidants, Free Radicals, Glutaredoxins, Glutathione, Peroxiredoxins, Reactive Oxygen Species, Superoxide Dismutase, Thioredoxins.
- diagnosis : Neoplasms.
- drug effects : Homeostasis.
- drug therapy : Neoplasms.
- metabolism : Neoplasms.
- chemical , pharmacology : Radiation-Sensitizing Agents.
- physiology : Radiation Tolerance.
- radiotherapy : Neoplasms.
- Dietary Supplements, Humans, Oxidation-Reduction, Prognosis, Signal Transduction.
Abstract
Although conventional radiotherapy can directly damage DNA and other organic molecules within cells, most of the damage and the cytotoxicity of such ionising radiation, comes from the production of ions and free radicals produced via interactions with water. This 'indirect effect', a form of oxidative stress, can be modulated by a variety of systems within cells that are in place to, in normal situations, maintain homeostasis and redox balance. If cancer cells express high levels of antioxidant redox proteins, they may be more resistant to radiation and so targeting such systems may be a profitable strategy to increase therapeutic efficacy of conventional radiotherapy. An overview, with exemplars, of the main systems regulating redox homeostasis is supplied and discussed in relation to their use as prognostic and predictive biomarkers, and how targeting such proteins and systems may increase radiosensitivity and, potentially, improve the radiotherapeutic response.
DOI: 10.1016/j.clon.2014.02.003
PubMed: 24581945
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Zhang</name><affiliation wicri:level="4"><nlm:affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham</wicri:regionArea><orgName type="university">Université de Nottingham</orgName><placeName><settlement type="city">Nottingham</settlement><region type="nation">Angleterre</region><region type="région" nuts="1">Nottinghamshire</region></placeName></affiliation></author><author><name sortKey="Martin, S G" sort="Martin, S G" uniqKey="Martin S" first="S G" last="Martin">S G Martin</name><affiliation wicri:level="4"><nlm:affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK. 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Zhang</name><affiliation wicri:level="4"><nlm:affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham</wicri:regionArea><orgName type="university">Université de Nottingham</orgName><placeName><settlement type="city">Nottingham</settlement><region type="nation">Angleterre</region><region type="région" nuts="1">Nottinghamshire</region></placeName></affiliation></author><author><name sortKey="Martin, S G" sort="Martin, S G" uniqKey="Martin S" first="S G" last="Martin">S G Martin</name><affiliation wicri:level="4"><nlm:affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK. Electronic address: stewart.martin@nottingham.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham</wicri:regionArea><orgName type="university">Université de Nottingham</orgName><placeName><settlement type="city">Nottingham</settlement><region type="nation">Angleterre</region><region type="région" nuts="1">Nottinghamshire</region></placeName></affiliation></author></analytic><series><title level="j">Clinical oncology (Royal College of Radiologists (Great Britain))</title><idno type="eISSN">1433-2981</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidants (metabolism)</term><term>Dietary Supplements (MeSH)</term><term>Free Radicals (metabolism)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (metabolism)</term><term>Homeostasis (drug effects)</term><term>Humans (MeSH)</term><term>Neoplasms (diagnosis)</term><term>Neoplasms (drug therapy)</term><term>Neoplasms (metabolism)</term><term>Neoplasms (radiotherapy)</term><term>Oxidation-Reduction (MeSH)</term><term>Peroxiredoxins (metabolism)</term><term>Prognosis (MeSH)</term><term>Radiation Tolerance (physiology)</term><term>Radiation-Sensitizing Agents (pharmacology)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Superoxide Dismutase (metabolism)</term><term>Thioredoxins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antioxydants (métabolisme)</term><term>Compléments alimentaires (MeSH)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Homéostasie (effets des médicaments et des substances chimiques)</term><term>Humains (MeSH)</term><term>Oxydoréduction (MeSH)</term><term>Peroxirédoxines (métabolisme)</term><term>Pronostic (MeSH)</term><term>Radicaux libres (métabolisme)</term><term>Radiosensibilisants (pharmacologie)</term><term>Radiotolérance (physiologie)</term><term>Superoxide dismutase (métabolisme)</term><term>Thiorédoxines (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>Tumeurs (diagnostic)</term><term>Tumeurs (métabolisme)</term><term>Tumeurs (radiothérapie)</term><term>Tumeurs (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antioxidants</term><term>Free Radicals</term><term>Glutaredoxins</term><term>Glutathione</term><term>Peroxiredoxins</term><term>Reactive Oxygen Species</term><term>Superoxide Dismutase</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Homeostasis</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Homéostasie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antioxydants</term><term>Espèces réactives de l'oxygène</term><term>Glutarédoxines</term><term>Glutathion</term><term>Peroxirédoxines</term><term>Radicaux libres</term><term>Superoxide dismutase</term><term>Thiorédoxines</term><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Radiosensibilisants</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Radiation-Sensitizing Agents</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Radiotolérance</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Radiation Tolerance</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="radiothérapie" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Dietary Supplements</term><term>Humans</term><term>Oxidation-Reduction</term><term>Prognosis</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Compléments alimentaires</term><term>Humains</term><term>Oxydoréduction</term><term>Pronostic</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although conventional radiotherapy can directly damage DNA and other organic molecules within cells, most of the damage and the cytotoxicity of such ionising radiation, comes from the production of ions and free radicals produced via interactions with water. This 'indirect effect', a form of oxidative stress, can be modulated by a variety of systems within cells that are in place to, in normal situations, maintain homeostasis and redox balance. If cancer cells express high levels of antioxidant redox proteins, they may be more resistant to radiation and so targeting such systems may be a profitable strategy to increase therapeutic efficacy of conventional radiotherapy. An overview, with exemplars, of the main systems regulating redox homeostasis is supplied and discussed in relation to their use as prognostic and predictive biomarkers, and how targeting such proteins and systems may increase radiosensitivity and, potentially, improve the radiotherapeutic response. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24581945</PMID><DateCompleted><Year>2014</Year><Month>11</Month><Day>25</Day></DateCompleted><DateRevised><Year>2014</Year><Month>04</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1433-2981</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>5</Issue><PubDate><Year>2014</Year><Month>May</Month></PubDate></JournalIssue><Title>Clinical oncology (Royal College of Radiologists (Great Britain))</Title><ISOAbbreviation>Clin Oncol (R Coll Radiol)</ISOAbbreviation></Journal><ArticleTitle>Redox proteins and radiotherapy.</ArticleTitle><Pagination><MedlinePgn>289-300</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.clon.2014.02.003</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0936-6555(14)00070-3</ELocationID><Abstract><AbstractText>Although conventional radiotherapy can directly damage DNA and other organic molecules within cells, most of the damage and the cytotoxicity of such ionising radiation, comes from the production of ions and free radicals produced via interactions with water. This 'indirect effect', a form of oxidative stress, can be modulated by a variety of systems within cells that are in place to, in normal situations, maintain homeostasis and redox balance. If cancer cells express high levels of antioxidant redox proteins, they may be more resistant to radiation and so targeting such systems may be a profitable strategy to increase therapeutic efficacy of conventional radiotherapy. An overview, with exemplars, of the main systems regulating redox homeostasis is supplied and discussed in relation to their use as prognostic and predictive biomarkers, and how targeting such proteins and systems may increase radiosensitivity and, potentially, improve the radiotherapeutic response. </AbstractText><CopyrightInformation>Copyright © 2014 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>S G</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Academic Unit of Clinical Oncology, University of Nottingham, School of Medicine, Nottingham University Hospitals NHS Trust, City Hospital Campus, Nottingham, UK. Electronic address: stewart.martin@nottingham.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>02</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Clin Oncol (R Coll Radiol)</MedlineTA><NlmUniqueID>9002902</NlmUniqueID><ISSNLinking>0936-6555</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019587" MajorTopicYN="N">Dietary Supplements</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005609" MajorTopicYN="N">Free Radicals</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009369" MajorTopicYN="N">Neoplasms</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000532" MajorTopicYN="Y">radiotherapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054464" MajorTopicYN="N">Peroxiredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011836" MajorTopicYN="N">Radiation Tolerance</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011838" MajorTopicYN="N">Radiation-Sensitizing Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Radiosensitivity</Keyword><Keyword MajorTopicYN="N">radiotherapy</Keyword><Keyword MajorTopicYN="N">reactive oxygen species</Keyword><Keyword MajorTopicYN="N">redox homeostasis</Keyword><Keyword MajorTopicYN="N">redox imaging</Keyword><Keyword MajorTopicYN="N">redox proteins</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>11</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>01</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>02</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>3</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>3</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24581945</ArticleId><ArticleId IdType="pii">S0936-6555(14)00070-3</ArticleId><ArticleId IdType="doi">10.1016/j.clon.2014.02.003</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Nottinghamshire</li></region><settlement><li>Nottingham</li></settlement><orgName><li>Université de Nottingham</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Zhang, Y" sort="Zhang, Y" uniqKey="Zhang Y" first="Y" last="Zhang">Y. 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