作者: Eunice C. Chan , Shui Y. Lam , Kin H. Fu , Yok L. Kwong
DOI: 10.1016/J.CANCERGENCYTO.2005.03.008
关键词: Cancer research 、 XRCC1 、 GSTP1 、 Allele 、 Biology 、 Lung cancer 、 Molecular biology 、 Retinoic acid receptor beta 、 Carcinogenesis 、 Methylation 、 Methyltransferase
摘要: Abstract An association between functional polymorphisms of genes resulting in decreased detoxification carcinogens or DNA repair and aberrant promoter methylation is an attractive hypothesis lung carcinogenesis. The genotypes at polymorphic sites the glutathione S-transferase ( GST ) M1 (null/wildtype) P1 (nucleotide 2627 A/G), myeloperoxidase MPO −463 G/A), X-ray cross-complementing group 1 XRCC1 (nucleotides 26304 C/T; 28152 NADPH quinine oxidoreductase NQO1 609 C/T) 75 Chinese patients with non-small cell cancer (NSCLC) were characterized polymerase chain reaction–restriction fragment length polymorphism. Results correlated CDKN2A (alias p16 INK4A ), retinoic acid receptor beta RARB methylguanine-DNA methyltransferase MGMT death-associated-protein DAP kinase tumors. In comparison age-matched control, none associated increased risks. male patients, however, GG homozygous state was (odds ratio OR=3.63, 95% confidence interval CI=1.26–10.51), T allele heterozygous/homozygous (OR=6.13, CI=1.55–24.16) (OR=7.67, CI=1.62–36.18). female GSTP1 G (OR=18.0, CI=0.76–427.29). These results showed that deficiencies metabolic pathways protect cells from carcinogen induced damage might be linked to during