title: Genetic Polymorphism of Epoxide Hydrolase and GSTM1 in Lung Cancer Susceptibility of Korean Population.
abstract: OBJECTIVE
  Although 80~90% of patients with lung cancer are smokers, only 11% of smokers develop lung cancer. Genetic susceptibility according to the polymorphism of the epoxide hydrolase (mEPHX) gene and homozygous deletion of GSTM1 (M1 subunit of Glutathione S transferase) was studied in this case control study.
  
  
  METHODS
  Genomic DNA from 76 subjects with lung cancer (40 squamous cell carcinoma, 13 adenocarcinoma, 10 subtype undetermined non-small cell lung cancer, and 13 small cell lung carcinoma) and 62 age- matched controls were extracted from peripheral white blood cells. PCR and RFLP (restriction fragments length polymorphism) with restriction enzyme (RsaI) and automatic sequencing were used for mEPHX genotyping (T-->C, Tyr113His) in exon 3 and (A-->G, His139Arg) in exon 4. Looking for homozygous deletions of GSTM1, multiplex PCR with primers for the GSTM1 gene and coagulation factor V gene (as positive control) were performed.
  
  
  RESULTS
  The age distribution between the cancer and control groups were similar (63.6 7.2 vs. 61.1 7.9 years). The lung cancer group, however, had more smokers (73.3%, 44/60) than the control group (21/54, 38.9%, p<0.001). The rate of homozygous deletion of the GSTM1 gene was significantly higher in the lung cancer group (65.8%, 50/76) than in the control group (46.8%, 29/62, p<0.05), causing the relative risk of GSTM1 deletion for lung cancer as 2.19 (95% CI: 1.10~4.35, p=0.02). Among 118 subjects whose mEPHX gene polymorphisms were studied, 62 (52.5%) subjects showed genotypes with slow enzyme activity while 45 (38.1%) showed normal enzyme activity and 11 (9.3%) showed fast enzyme activity. There was no significant difference in the distribution of mEPHX gene polymorphisms between the two groups.
  
  
  CONCLUSIONS
  The homozygous deletion of the GSTM1 gene was associated with high lung cancer susceptibility, whereas the mEPHX genotype showed no significant connection with risk of lung cancer in a sample Korean population.
authors.forename: Jun Hwa
authors.initials: JH
authors.lastname: Hwang
authors.forename: Kyu Sik
authors.initials: KS
authors.lastname: Kim
authors.forename: Yu Il
authors.initials: YI
authors.lastname: Kim
authors.forename: Eun Joung
authors.initials: EJ
authors.lastname: Kim
authors.forename: Kyung Hwa
authors.initials: KH
authors.lastname: Park
authors.forename: Gye Jung
authors.initials: GJ
authors.lastname: Cho
authors.forename: Jin Young
authors.initials: JY
authors.lastname: Ju
authors.forename: Sung Chul
authors.initials: SC
authors.lastname: Lim
authors.forename: Young Chul
authors.initials: YC
authors.lastname: Kim
authors.forename: Kyung Ok
authors.initials: KO
authors.lastname: Park
authors.forename: Jong Tae
authors.initials: JT
authors.lastname: Park
authors.forename: Sung Ja
authors.initials: SJ
authors.lastname: Ahn
keywords: Epoxide hydrolase; Genetic polymorphism; Glutathione S transferase; Lung neoplasm