To determine the extent of promoter hypermethylation in early lung tumorigenesis, we analyzed promoter methylation status of the p16, death-associated protein kinase (DAPK) and glutathione S-transferase P1 (GSTP1) genes

TIMP3, DAPK1 and AKR1B10 are important for squamous cell lung cancer tumorogenesis while AKR1B10 is potential oncogene whereas TIMP3 and DAPK1 are potential tumor suppressor genes.

results showed RASSF1A & DAPK genes' promoter methylation occurred frequently in lung tumors, although prevalence of this alteration in these genes was not associated with smoking status of the patients or occurrence of mutations in K-ras, p53 & EGFR

p16INK4A, DAPK1, PTEN and MT1G genes were not frequently methylated in the stage I non-small cell lung cancer in China.

Loss of Med1 expression directly correlates with a loss of dapk1 expression in a number of human lung cancers and cancer cell lines.

Hypermethylation of DAPK was significantly associated with shorter time to recurrence of nonsmall cell lung cancer.

Promoter hypermethylation of RASSF1A, p16, and DAPK genes was detected in lung cancer.

Combined effects of cigarette smoke and hypermethylations of DAPK are associated with non small cell lung cancer.

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.

The frequency of DAPK methylation was significantly higher in lung cancer than in non-malignant lung tissues.

[The role of lung cancer related gene methylation in the early diagnosis of lung cancer].