Original Article
Promoter methylation of p16 and DAPK genes in brushing, blood, and tissue samples from patients with nasopharyngeal carcinoma: a systematic meta-analysis
Abstract
Background: Promoter methylation of tumor suppressor genes (TSGs) p16 and death-associated protein kinase (DAPK) has been reported in various carcinomas. However, the correlation between p16 or DAPK promoter methylation and the detection of nasopharyngeal carcinoma (NPC) in different sample types remains unclear.
Methods: A systematic literature research was conducted to identify available studies. The pooled odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated and analyzed.
Results: Eleven eligible papers on p16 promoter methylation and seven eligible papers on DAPK promoter methylation were included in this analysis. The pooled OR of p16 and DAPK promoter methylation was significantly higher in samples of NPC tissues than in nontumorous (OR =5.49, P<0.001; OR =17.51, P<0.001; respectively). Moreover, the pooled OR of p16 promoter methylation was significantly higher in NPC than in normal blood and noncancerous brushing samples (OR =19.37, P<0.001; OR =15.03, P<0.001; respectively). In NPC samples, the OR of DAPK promoter methylation were significantly higher than in normal blood and normal brushing samples (OR =7.23, P<0.001; OR =42.00, P=0.001; respectively). No significant correlation was found between p16 or DAPK promoter methylation and clinical stage (P>0.1).
Conclusions: Our findings suggested that p16 and DAPK promoter methylation may be associated with the carcinogenesis of NPC. Promoter methylation of p16 or DAPK may become a noninvasive biomarker for NPC detection in blood and brushing samples. DAPK or p16 promoter methylation was not correlated with tumor stage. Conducting additional studies is essential in the future to confirm our results.
Methods: A systematic literature research was conducted to identify available studies. The pooled odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated and analyzed.
Results: Eleven eligible papers on p16 promoter methylation and seven eligible papers on DAPK promoter methylation were included in this analysis. The pooled OR of p16 and DAPK promoter methylation was significantly higher in samples of NPC tissues than in nontumorous (OR =5.49, P<0.001; OR =17.51, P<0.001; respectively). Moreover, the pooled OR of p16 promoter methylation was significantly higher in NPC than in normal blood and noncancerous brushing samples (OR =19.37, P<0.001; OR =15.03, P<0.001; respectively). In NPC samples, the OR of DAPK promoter methylation were significantly higher than in normal blood and normal brushing samples (OR =7.23, P<0.001; OR =42.00, P=0.001; respectively). No significant correlation was found between p16 or DAPK promoter methylation and clinical stage (P>0.1).
Conclusions: Our findings suggested that p16 and DAPK promoter methylation may be associated with the carcinogenesis of NPC. Promoter methylation of p16 or DAPK may become a noninvasive biomarker for NPC detection in blood and brushing samples. DAPK or p16 promoter methylation was not correlated with tumor stage. Conducting additional studies is essential in the future to confirm our results.
