作者: Chikako Kiyohara , Koichi Takayama , Yoichi Nakanishi
DOI: 10.1016/J.LUNGCAN.2006.08.009
关键词:
摘要: Lung cancer is a major cause of cancer-related death in the developed countries and overall survival rate has still an extremely poor. Although cigarette smoking main lung cancer, not all smokers develop fraction lifelong non-smokers will die from cancer. Genetic host factors have recently been implicated to account for some observed differences susceptibility. Various DNA alterations can be caused by exposure environmental endogenous carcinogens. Most these alterations, if repaired, may result genetic instability, mutagenesis cell death. repair mechanisms are important maintaining integrity preventing carcinogenesis. Recent association studies on risk focused identifying effects single nucleotide polymorphisms (SNPs) candidate genes, among which genes increasingly studied. variations thought modulate capacity suggested related risk. We identified sufficient number epidemiologic conduct meta-analysis base (BER) pathway, focusing 8-oxoguanine glycosylase 1, X-ray cross-complementing group 1 (XRCC1) apurinic/apyrimidinic endonuclease 1. The 399Gln/Gln genotype XRCC1 Arg399Gln polymorphism was associated with increased Asians (OR=1.34, 95% CI=1.16-1.54) but Caucasians. Little evidence associations found between other BER Considering data available, it conjectured that there any SNP this increase/decrease probably minimal. Advances identification new high-throughput genotyping techniques facilitate analysis multiple pathways. Therefore, likely defining feature future simultaneous large samples cases controls.