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dc.contributor.authorZienolddiny, Sen_US
dc.contributor.authorCampa, Den_US
dc.contributor.authorLind, Hen_US
dc.contributor.authorRyberg, Den_US
dc.contributor.authorSkaug, Ven_US
dc.contributor.authorStangeland, Len_US
dc.contributor.authorPhillips, DHen_US
dc.contributor.authorCanzian, Fen_US
dc.contributor.authorHaugen, Aen_US
dc.date.accessioned2018-09-04T11:58:14Z
dc.date.issued2006-03en_US
dc.identifier3en_US
dc.identifier.citationCARCINOGENESIS, 2006, 27 pp. 560 - 567en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2544
dc.identifier.doi10.1093/carcin/bgi232en_US
dc.description.abstractLung cancer is a leading cause of cancer mortality with an inter-individual difference in susceptibility to the disease. The inheritance of low-efficiency genotypes involved in DNA repair and replication may contribute to the difference in susceptibility. We investigated 44 single nucleotide polymorphisms (SNPs) in 20 DNA repair genes including nucleotide excision repair (NER) genes XPA, ERCC1, ERCC2/XPD, ERCC4/XPF and ERCC5/XPG; base excision repair (BER) genes APE1/APEX, OGG1, MPG, XRCC1, PCNA, POLB, POL iota, LIG3 and EXO1; double-strand break repair (DSB-R) genes XRCC2, XRCC3, XRCC9, NBS1 and ATR; and direct damage reversal (DR) gene MGMT/AGT. The study included 343 non-small cell lung cancer (NSCLC) cases and 413 controls from Norwegian general population. Our results indicate that SNPs in the NER genes ERCC1 (Asn118Asn, 15310G > C, 8902G > T), XPA (-4G > A), ERCC2/XPD (Lys751Gln) and ERCC5/XPD (His46His); the BER genes APE1/APEX (Ile64Val), OGG1 (Ser326Cys), PCNA (1876A > G) and XRCC1 (Arg194Trp, Arg280His, Arg399Gln); and the DSB-R genes ATR (Thr211Met), NBS1 (Glu185Gln), XRCC2 (Arg188His) and XRCC9 (Thr297Ile) modulate NSCLC risk. The level of polycyclic aromatic hydrocarbon-DNA (PAH-DNA) adducts in normal lung tissue from 211 patients was analysed. The variant alleles of XRCC1(Arg280His), XRCC1 (Arg399Gln), ERCC1(G8092T), ERCC5(His46His) and MGMT/AGT(Lys178Arg) were more frequent in patients with PAH-DNA adduct levels lower than the mean whereas the XRCC1(Arg194Trp) variant was more frequent in cases with higher adduct levels than the mean.en_US
dc.format.extent560 - 567en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherOXFORD UNIV PRESSen_US
dc.titlePolymorphisms of DNA repair genes and risk of non-small cell lung canceren_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1093/carcin/bgi232en_US
rioxxterms.licenseref.startdate2006-03en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfCARCINOGENESISen_US
pubs.notesaffiliation: Haugen, A (Reprint Author), Natl Inst Occupat Hlth, Dept Toxicol, PB 8149, N-0033 Oslo, Norway. Natl Inst Occupat Hlth, Dept Toxicol, N-0033 Oslo, Norway. Haukeland Univ Hosp, N-5021 Bergen, Norway. Int Agcy Res Canc, Genome Anal Grp, F-69372 Lyon, France. Univ Pisa, Dept Sci Study Man & Environm, Pisa, Italy. Inst Canc Res, Sect Mol Carcinogenesis, Surrey SM2 5NG, England. keywords-plus: NUCLEOTIDE EXCISION-REPAIR; STRAND BREAK REPAIR; FUNCTIONAL-CHARACTERIZATION; XENOBIOTIC METABOLISM; XRCC3 POLYMORPHISMS; COLORECTAL-CANCER; XPD POLYMORPHISMS; DAMAGED DNA; IN-VIVO; SUSCEPTIBILITY research-areas: Oncology web-of-science-categories: Oncology author-email: age.haugen@stami.no researcherid-numbers: Zienolddiny, Shanbeh/O-7392-2015 Campa, Daniele/K-1617-2016 orcid-numbers: Campa, Daniele/0000-0003-3220-9944 Zienolddiny, Shan/0000-0001-9747-9625 Canzian, Federico/0000-0002-4261-4583 Phillips, David/0000-0001-8509-3485 number-of-cited-references: 61 times-cited: 302 usage-count-last-180-days: 0 usage-count-since-2013: 19 journal-iso: Carcinogenesis doc-delivery-number: 018NN unique-id: ISI:000235771300023 oa: gold_or_bronze da: 2018-09-04en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Human Biomonitoring & Carcinogen Activation
pubs.volume27en_US
pubs.embargo.termsNot knownen_US
icr.researchteamHuman Biomonitoring & Carcinogen Activationen_US
dc.contributor.icrauthorPhillips, David Hunteren_US


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