title: Association of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region.
abstract: OBJECTIVE
  To explore associations of CYP2E1 and NAT2 polymorphisms with lung cancer susceptibility among Mongolian and Han populations in the Inner Mongolian region.
  
  
  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.
authors.affiliation: Department of Pharmacology of Pharmaceutical College, Inner Mongolia Medical University, Hohhot, China E-mail : changfh@sina.com.
authors.forename: Jing-Wen
authors.initials: JW
authors.lastname: Zhang
authors.forename: Wan-Jia
authors.initials: WJ
authors.lastname: Yu
authors.forename: Xiao-Min
authors.initials: XM
authors.lastname: Sheng
authors.forename: Fu-Hou
authors.initials: FH
authors.lastname: Chang
authors.forename: Tu-Ya
authors.initials: TY
authors.lastname: Bai
authors.forename: Xiao-Li
authors.initials: XL
authors.lastname: Lv
authors.forename: Guang
authors.initials: G
authors.lastname: Wang
authors.forename: Su-Zhen
authors.initials: SZ
authors.lastname: Liu
mesh_terms: D000107:Acetylation; D000483:Alleles; D001191:Arylamine N-Acetyltransferase / Q000235:genetics* / Q000378:metabolism; D002277:Carcinoma / Q000208:ethnology / Q000235:genetics*; D016022:Case-Control Studies; D002681:China / Q000453:epidemiology / Q000208:ethnology; D019392:Cytochrome P-450 CYP2E1 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008175:Lung Neoplasms / Q000208:ethnology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012907:Smoking / Q000453:epidemiology / Q000378:metabolism
chemical_list: D019392:Cytochrome P-450 CYP2E1; D001191:Arylamine N-Acetyltransferase; C478900:NAT2 protein, human