Association between the risk for lung adenocarcinoma and a (−4) G-to-A polymorphism in the XPA gene

• Verfasst von: Butkiewicz, Dorota [VerfasserIn]
• Verfasst von: Popanda, Odilia [VerfasserIn]
• Verfasst von: Risch, Angela [VerfasserIn]
• Verfasst von: Edler, Lutz [VerfasserIn]
• Verfasst von: Dienemann, Hendrik [VerfasserIn]
• Verfasst von: Schulz, Volker [VerfasserIn]
• Verfasst von: Kayser, Klaus [VerfasserIn]
• Verfasst von: Drings, Peter [VerfasserIn]
• Verfasst von: Bartsch, Helmut [VerfasserIn]
• Verfasst von: Schmezer, Peter [VerfasserIn]
• 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
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1742217001

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.