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dc.contributor.authorMollerup, Sen_US
dc.contributor.authorBerge, Gen_US
dc.contributor.authorBaera, Ren_US
dc.contributor.authorSkaug, Ven_US
dc.contributor.authorHewer, Aen_US
dc.contributor.authorPhillips, DHen_US
dc.contributor.authorStangeland, Len_US
dc.contributor.authorHaugen, Aen_US
dc.date.accessioned2018-09-03T13:05:53Z
dc.date.issued2006-08-15en_US
dc.identifier4en_US
dc.identifier.citationINTERNATIONAL JOURNAL OF CANCER, 2006, 119 pp. 741 - 744en_US
dc.identifier.issn0020-7136en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2515
dc.identifier.doi10.1002/ijc.21891en_US
dc.description.abstractIt is controversial whether women have a higher lung cancer susceptibility compared to men. We previously reported higher levels of smoking-related bulky DNA adducts in female lungs. In a pilot study (27 cases), we also found a higher level of female lung cytochrome P4501A1 (CYP1A1) gene expression. In the present extended study we report oil the pulmonary expression of several genes involved in polycyclic aromatic hydrocarbon bioactivation in relation to sex, smoking and DNA adducts. CYP1A1, CYP1B1, aryl hydrocarbon receptor and microsomal epoxide hydrolase gene expression was measured by quantitative real-time reverse transcriptase-PCR in 121 normal lung tissue samples. The expression of CYP1A1 and CYP1B1 was significantly higher among current smokers compared to ex-smokers and never-smokers. Among current smokers, females had a 3.9-fold higher median level of CYP1A1 compared to males (p = 0.011). CYP1B1 expression was not related to sex. Lung DNA adducts (measured by P-32-postlabeling) were highly significantly related to CYP1A1 (P < 0.0001) irrespective of smoking-status. Our results are consistent with the hypothesis that CYP1A1 plays a significant role in lung DNA adduct formation and support a higher susceptibility to long cancer among females. (c) 2006 Wiley-Liss, Inc.en_US
dc.format.extent741 - 744en_US
dc.languageEnglishen_US
dc.language.isoEnglishen_US
dc.publisherWILEY-LISSen_US
dc.titleSex differences in risk of lung cancer: Expression of genes in the PAH bioactivation pathway in relation to smoking and bulky DNA adductsen_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1002/ijc.21891en_US
rioxxterms.licenseref.startdate2006-08-15en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfINTERNATIONAL JOURNAL OF CANCERen_US
pubs.notesaffiliation: Mollerup, S (Reprint Author), Natl Inst Occupat Hlth, Dept Toxicol, N-0033 Oslo, Norway. Natl Inst Occupat Hlth, Dept Toxicol, N-0033 Oslo, Norway. Haukeland Hosp, N-5021 Bergen, Norway. keywords: lung cancer; sex differences; cytochrome P450; DNA adducts keywords-plus: TOBACCO CARCINOGENS; GENDER-DIFFERENCES; ESTROGEN-RECEPTOR; WOMEN; SUSCEPTIBILITY; MUTATIONS; GEFITINIB; TISSUE; MEN research-areas: Oncology web-of-science-categories: Oncology author-email: [email protected] orcid-numbers: Phillips, David/0000-0001-8509-3485 cited-references: Bain C, 2004, J NATL CANCER I, V96, P826, DOI 10.1093/jnci/djh143. Berge G, 2004, LUNG CANCER-J IASLC, V45, P289, DOI 10.1016/j.lungcan.2004.02.014. Denissenko MF, 1996, SCIENCE, V274, P430, DOI 10.1126/science.274.5286.430. Dresler CM, 2000, LUNG CANCER-J IASLC, V30, P153, DOI 10.1016/S0169-5002(00)00163-X. Haugen A, 2002, CARCINOGENESIS, V23, P227, DOI 10.1093/carcin/23.2.227. Hecht SS, 2003, NAT REV CANCER, V3, P733, DOI 10.1038/nrc1190. Henschke CI, 2004, LUNG CANCER-J IASLC, V43, P1, DOI 10.1016/j.lungcan.2003.08.024. Jemal A, 2004, CA-CANCER J CLIN, V54, P8, DOI 10.3322/canjclin.54.1.8. Kreuzer M, 2000, BRIT J CANCER, V82, P227. Lynch TJ, 2004, NEW ENGL J MED, V350, P2129, DOI 10.1056/NEJMoa040938. MCLEMORE TL, 1990, J NATL CANCER I, V82, P1333, DOI 10.1093/jnci/82.16.1333. Mollerup S, 1999, CANCER RES, V59, P3317. Mollerup S, 2002, LUNG CANCER-J IASLC, V37, P153, DOI 10.1016/S0169-5002(02)00039-9. Nelson HH, 1999, J NATL CANCER I, V91, P2032, DOI 10.1093/jnci/91.23.2032. Paez JG, 2004, SCIENCE, V304, P1497, DOI 10.1126/science.1099314. RISCH HA, 1993, AM J EPIDEMIOL, V138, P281, DOI 10.1093/oxfordjournals.aje.a116857. RYBERG D, 1994, CANCER RES, V54, P5801. Shigematsu H, 2005, J NATL CANCER I, V97, P339, DOI 10.1093/jnci/dji055. Shriver SP, 2000, JNCI-J NATL CANCER I, V92, P24, DOI 10.1093/jnci/92.1.24. Tang DL, 2001, CANCER RES, V61, P6708. Toyooka S, 2003, HUM MUTAT, V21, P229, DOI 10.1002/humu.10177. Veglia F, 2003, CANCER EPIDEM BIOMAR, V12, P157. Wei QY, 2000, J NATL CANCER I, V92, P1764. Zang EA, 1996, J NATL CANCER I, V88, P183, DOI 10.1093/jnci/88.3-4.183. number-of-cited-references: 24 times-cited: 74 usage-count-last-180-days: 0 usage-count-since-2013: 5 journal-iso: Int. J. Cancer doc-delivery-number: 063AR unique-id: ISI:000238988800003 oa: gold_or_bronze da: 2018-09-03en_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.volume119en_US
pubs.embargo.termsNot knownen_US
icr.researchteamHuman Biomonitoring & Carcinogen Activationen_US
dc.contributor.icrauthorPhillips, David Hunteren_US


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