Journal Article

XPA polymorphism associated with reduced lung cancer risk and a modulating effect on nucleotide excision repair capacity

Xifeng Wu, Hua Zhao, Qingyi Wei, Christopher I. Amos, Kerang Zhang, Zhaozheng Guo, Yawei Qiao, Waun K. Hong and Margaret R. Spitz

in Carcinogenesis

Volume 24, issue 3, pages 505-509
Published in print March 2003 | ISSN: 0143-3334
Published online March 2003 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/24.3.505
XPA polymorphism associated with reduced lung cancer risk and a modulating effect on nucleotide excision repair capacity

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XPA, a DNA binding protein in the nucleotide excision repair (NER) pathway, modulates damage recognition. Recently, a common single-nucleotide polymorphism (A → G) of unknown function was identified in the 5′ non-coding region of the XPA gene. Because a deficiency in NER is associated with an increased risk of lung cancer, we evaluated the role of this polymorphism in 695 lung cancer case patients and 695 age-, sex-, ethnicity- and smoking-matched control subjects. We also studied the effect of this polymorphism on NER capacity in a subset sample for whom the host cell reactivation data were available. The presence of one or two copies of the G allele was associated with a reduced lung cancer risk for Caucasians {adjusted odds ratio (ORadj) = 0.69 [95% confidence interval (CI) = 0.53–0.90]}, Mexican-Americans [ORadj = 0.32 (95% CI = 0.12–0.83)] and African-Americans [ORadj = 0.45 (95% CI = 0.16–1.22)]. In Caucasians, ever smokers with one or more copies of the G allele were observed to have a significantly reduced risk of lung cancer. Control subjects with one or two copies of the G allele demonstrated more efficient DRC than did those with the homozygous A allele. Our data suggest that the XPA 5′ non-coding region polymorphism modulates NER capacity and is associated with decreased lung cancer risk, especially in the presence of exposure to tobacco carcinogens.

Keywords: DRC, DNA repair capacity; NER, nucleotide excision repair

Journal Article.  4552 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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