title: [Relationship between promoter methylation of p16, DAPK and RAR beta genes and the clinical data of non-small cell lung cancer].
abstract: OBJECTIVE
  To investigate the effects of promoter methylation of p16, death-associated protein kinase (DAPK) and retinoic acid receptor-beta (RAR beta) genes on clinical data in non-small cell lung cancers, and to study the effect of smoking on the risk of gene methylation.
  
  
  METHODS
  The promoter methylation of p16, DAPK and RAR beta genes in 200 primary non-small cell lung cancers and the corresponding nonmalignant lung tissues were determined by methylation-specific PCR.
  
  
  RESULTS
  Methylation in the tumor tissues was detected in 51.0% for p16, 60.0% for DAPK, and 58.0% for RAR beta gene, with significant differences (P < 0.05) when compared with those in the corresponding nonmalignant tissues(12.5%, 11.5% and 15.0%) respectively. p16 gene methylation in tumor tissue was associated with age significantly in unconditional logistic regression analysis (P < 0.01) and histologic type (P < 0.05). DAPK gene methylation in tumor tissue was associated significantly with age (P < 0.05), gender (P < 0.05) and clinical type (P < 0.05). RAR beta gene methylation in tumor tissue was associated with clinical type (P < 0.05) and tumor stage (P < 0.05) significantly. The interaction odds ratio (OR) for the gene-gene interaction in tumor tissue between p16 and DAPK was 1.987 (95%CI:1.055-3.743). The results of the gene-smoking analyses revealed that a relationship existed between cigarette smoking and p16 gene methylation (OR = 3.139, 95%CI: 1.046-9.419), the OR for the relationship of DAPK gene methylation and cigarette smoking was 3.585(95%CI: 1.270-10.123) in tumor tissue. The RAR beta gene methylation did not differ based on the smoking status of patients in tumor tissue.
  
  
  CONCLUSIONS
  The p16, DAPK and RAR beta genes methylation are strongly associated with clinical data of non-small cell lung cancer, and methylation of p16 and DAPK genes are associated with tobacco smoking.
authors.affiliation: Environment Epigenetic Laboratory, Institute of Environmental Health, College of Public Health, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310058 PR China.
authors.forename: Chen-ye
authors.initials: CY
authors.lastname: Zhang
authors.forename: Yong-tang
authors.initials: YT
authors.lastname: Jin
authors.forename: He-yun
authors.initials: HY
authors.lastname: Xu
authors.forename: Hu
authors.initials: H
authors.lastname: Zhang
authors.forename: Wei-min
authors.initials: WM
authors.lastname: Zhang
authors.forename: Xiao-yu
authors.initials: XY
authors.lastname: Sun
authors.forename: Cong
authors.initials: C
authors.lastname: Tan
authors.forename: Chun-mei
authors.initials: CM
authors.lastname: Chen
mesh_terms: D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000235:genetics*; D002289:Carcinoma, Non-Small-Cell Lung / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D019175:DNA Methylation; D064550:Death-Associated Protein Kinases; D019942:Genes, p16; D016015:Logistic Models; D008175:Lung Neoplasms / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D009367:Neoplasm Staging; D011401:Promoter Regions, Genetic; D018168:Receptors, Retinoic Acid / Q000235:genetics*; D012907:Smoking / Q000009:adverse effects
chemical_list: D051017:Apoptosis Regulatory Proteins; D018168:Receptors, Retinoic Acid; C082925:retinoic acid receptor beta; D064550:Death-Associated Protein Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases