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Verfasst von:Butkiewicz, Dorota [VerfasserIn]   i
 Popanda, Odilia [VerfasserIn]   i
 Risch, Angela [VerfasserIn]   i
 Edler, Lutz [VerfasserIn]   i
 Dienemann, Hendrik [VerfasserIn]   i
 Schulz, Volker [VerfasserIn]   i
 Kayser, Klaus [VerfasserIn]   i
 Drings, Peter [VerfasserIn]   i
 Bartsch, Helmut [VerfasserIn]   i
 Schmezer, Peter [VerfasserIn]   i
Titel:Association between the risk for lung adenocarcinoma and a (−4) G-to-A polymorphism in the XPA gene
Verf.angabe:Dorota Butkiewicz, Odilia Popanda, Angela Risch, Lutz Edler, Hendrik Dienemann, Volker Schulz, Klaus Kayser, Peter Drings, Helmut Bartsch, and Peter Schmezer
E-Jahr:2004
Jahr:December 2004
Umfang:6 S.
Fussnoten:Gesehen am 07.12.2020
Titel Quelle:Enthalten in: Cancer epidemiology, biomarkers & prevention
Ort Quelle:Philadelphia, Pa. : AACR, 1991
Jahr Quelle:2004
Band/Heft Quelle:13(2004), 12, Seite 2242-2246
ISSN Quelle:1538-7755
Abstract:Polymorphisms of genes coding for DNA repair can affect lung cancer risk. A common single nucleotide (−4) G-to-A polymorphism was identified previously in the 5′ untranslated region of the XPA gene. In a case-control study in European Caucasians, the influence of this polymorphism on primary lung cancer risk overall and according to histologic subtypes was investigated. Four hundred sixty-three lung cancer cases (including 204 adenocarcinoma and 212 squamous cell carcinoma) and 460 tumor-free hospital controls were investigated using PCR amplification and melting point analysis of sequence-specific hybridization probes. Odds ratios (OR) were calculated by multiple logistic regression analysis adjusting for age, gender, smoking habits, and occupational exposure and showed a slightly enhanced risk for all lung cancer cases as well as for squamous cell carcinoma and adenocarcinoma cases. Gene-environment interactions were analyzed with respect to smoking and occupational exposure. A nearly 3-fold increased risk for adenocarcinoma associated with the XPA AA genotype was observed for occupationally exposed individuals (OR, 2.95; 95% confidence interval, 1.42-6.14) and for heavy smokers (OR, 2.52; 95% confidence interval, 1.17-5.42). No genotype-dependent increase in OR was found for nonexposed individuals or those smoking <20 pack-years. The significant effect of the XPA polymorphism in heavy smokers and occupationally exposed individuals suggests an important gene-environment interaction for the XPA gene. The underlying mechanisms as to why AA homozygotes are predisposed to lung adenocarcinoma and which specific carcinogens are involved remains to be determined.
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Volltext: https://cebp.aacrjournals.org/content/13/12/2242
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1742217001
Verknüpfungen:→ Zeitschrift

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