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  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/21415
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dc.contributor.authorTrizna, Z.en
dc.contributor.authorde Andrade, M.en
dc.contributor.authorKyritsis, A. P.en
dc.contributor.authorBriggs, K.en
dc.contributor.authorLevin, V. A.en
dc.contributor.authorBruner, J. M.en
dc.contributor.authorWei, Q.en
dc.contributor.authorBondy, M. L.en
dc.date.accessioned2015-11-24T19:14:54Z-
dc.date.available2015-11-24T19:14:54Z-
dc.identifier.issn1055-9965-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21415-
dc.rightsDefault Licence-
dc.subjectAdulten
dc.subjectArylamine N-Acetyltransferase/*geneticsen
dc.subjectBrain Neoplasms/*enzymology/geneticsen
dc.subjectCase-Control Studiesen
dc.subjectCytochrome P-450 CYP1A1/*geneticsen
dc.subjectDNA Primersen
dc.subjectFemaleen
dc.subjectGlioma/*enzymology/geneticsen
dc.subjectGlutathione Transferase/*geneticsen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectOdds Ratioen
dc.subjectPilot Projectsen
dc.subjectPolymerase Chain Reactionen
dc.subjectPolymorphism, Geneticen
dc.subjectPrevalenceen
dc.subjectRisken
dc.subjectRisk Factorsen
dc.subjectTexasen
dc.titleGenetic polymorphisms in glutathione S-transferase mu and theta, N-acetyltransferase, and CYP1A1 and risk of gliomasen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/9641501-
heal.identifier.secondaryhttp://cebp.aacrjournals.org/content/7/6/553.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1998-
heal.abstractThe role of genetic polymorphisms in modulating susceptibility to carcinogenic exposures has been well explored for tobacco-related neoplasms but not for other neoplasms including gliomas. It is relevant to explore these polymorphisms because certain carcinogenic exposures such as nitrosamines are implicated in the risk of gliomas. We therefore conducted a pilot case-control study to examine the role of polymorphisms in GSTM1, GSTT1, NAT2 (rapid, intermediate, and slow acetylation), and CYP1A1 and risk of glioma. Ninety patients diagnosed with glioma were ascertained as part of an ongoing genetic epidemiological study and were age, gender, and race matched with 90 healthy controls. We used PCR based methodology to determine the prevalence of the above genetic polymorphisms using sequences and PCR conditions directly adapted from studies reported previously. We calculated univariate odds ratios and performed multiple logistic regression to assess interactions between polymorphisms. We found no statistically significant associations between the null genotypes of GSTM1 and GSTT1, and CYP1A1 and risk of gliomas. However, there was an intriguing pattern with NAT2 acetylation status (odds ratios, 1.81, 1.34, and 0.61 for rapid, intermediate, and slow acetylation, respectively; P = 0.10 for trend). It is unlikely that any single polymorphism is sufficiently predictive of risk, and a panel of markers integrated with epidemiological data should be conducted on a large number of study subjects to fully understand the role of genetic polymorphisms and brain tumor risk.en
heal.journalNameCancer Epidemiol Biomarkers Preven
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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