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자료유형
학술저널
저자정보
Zhang, Jing-Wen (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Yu, Wan-Jia (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Sheng, Xiao-Min (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Chang, Fu-Hou (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Bai, Tu-Ya (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Lv, Xiao-Li (Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University) Wang, Guang (The First Affiliated Hospital, Inner Mongolia Medical University) Liu, Su-Zhen (Huimin District Hospital of Hohhot)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제21호
발행연도
2014.1
수록면
9,203 - 9,210 (8page)

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Purpose: To explore associations of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region. Materials and Methods: CYP2E1 and NAT2 polymorphisms were detected by PCR-RFLP in 930 lung cancer patients and 1000 controls. Results: (1) Disequilibrium of the distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations (p=0.031). (2) Lung cancer risk was higher in individuals with c1, D allele of CYP2E1 RsaI/PstI, DraI polymorphisms and slow acetylation of NAT2 (c1 compared with c2, OR=1.382, 95%CI: 1.178-1.587, p=0.003; D compared with C, OR=1.241, 95%CI: 1.053-1.419, P<0.001; slow acetylation compared with rapid acetylation, OR=1.359, 95%CI:1.042-1.768, p=0.056) (3) Compared with c2/c2 and rapid acetylation, c1/c1 together with slow acetylation synergetically increased risk of lung cancer 2.83 fold. (4) Smokers with CYP2E1 c1/c1, DD, and NAT2 slow acetylation have 2.365, 1.916, 1.841 fold lung cancer risk than others with c2/c2, CC and NAT2 rapid acetylation, respectively. (5) Han smokers with NAT2 slow acetylation have 1.974 fold lung cancer risk than others with rapid acetylation. Conclusions: Disequilibrium distribution of NAT2 polymorphism was found in lung cancer patients among Han and Mongolian populations. Besides, Han smokers with NAT2 slow acetylation may have higher lung cancer risk compared with rapid acetylation couterparts. CYP2E1 c1/c1, DD and NAT2 slow acetylation, especially combined with smoking, contributes to the development of lung cancer. CYP2E1 c1/c1 or DD genotype and NAT2 slow acetylation have strong synergistic action in increasing lung cancer risk.

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