Flow chart of studies included in the meta-analysis.

<p>Flow chart of studies included in the meta-analysis.</p

Characteristics of studies included in the meta-analysis of <i>DAPK</i> promoter methylation and HNSCC.

<p>Characteristics of studies included in the meta-analysis of <i>DAPK</i> promoter methylation and HNSCC.</p

Association between promoter methylation of <i>DAPK</i> gene and HNSCC: A meta-analysis

<div><p>Background</p><p>The death-associated protein kinase (<i>DAPK</i>) is a tumor suppressor gene, which is a mediator of cell death of INF-γ–induced apoptosis. Aberrant methylation of <i>DAPK</i> promoter has been reported in patients with head and neck squamous cell carcinoma (HNSCC). However, the results of these studies are inconsistent. Hence, the present study aimed to evaluate the association between the promoter methylation of <i>DAPK</i> gene and HNSCC.</p><p>Methods</p><p>Relevant studies were systematically searched in PubMed, Web of Science, Ovid, and Embase. The association between <i>DAPK</i> promoter methylation and HNSCC was assessed by odds ratio (ORs) and 95% confidence intervals (CI). To evaluate the potential sources of heterogeneity, we conducted the meta-regression analysis and subgroup analysis.</p><p>Results</p><p>Eighteen studies were finally included in the meta-analysis. The frequency of <i>DAPK</i> promoter methylation in patients with HNSCC was 4.09-fold higher than the non-cancerous controls (OR = 3.96, 95%CI = 2.26–6.95). A significant association between <i>DAPK</i> promoter methylation and HNSCC was found among the Asian region and the Non-Asia region (Asian region, OR = 4.43, 95% CI = 2.29–8.58; Non-Asia region, OR = 3.39, 95% CI = 1.18–9.78). In the control source, the significant association between <i>DAPK</i> promoter methylation and HNSCC was seen among the autologous group and the heterogeneous group (autologous group, OR = 2.71, 95% CI = 1.49–4.93; heterogeneous group, OR = 9.50, 95% CI = 2.98–30.27). <i>DAPK</i> promoter methylation was significantly correlated with alcohol status (OR = 1.85, 95% CI = 1.07–3.21).</p><p>Conclusion</p><p>The results of this meta-analysis suggested that aberrant methylation of <i>DAPK</i> promoter was associated with HNSCC.</p></div

Summary of the subgroup analysisin the meta-analysis of <i>DAPK</i> promoter methylation and HNSCC.

<p>Summary of the subgroup analysisin the meta-analysis of <i>DAPK</i> promoter methylation and HNSCC.</p

Forest plots of <i>DAPK</i> promoter methylation associated with HNSCC.

<p>Forest plots of <i>DAPK</i> promoter methylation associated with HNSCC.</p

Begg’s funnel plot of <i>DAPK</i> promoter methylation associated with HNSCC.

<p>Begg’s funnel plot of <i>DAPK</i> promoter methylation associated with HNSCC.</p

Characteristics of studies included in themeta-analysis of <i>DAPK</i> promoter methylation and clinicopathological features.

<p>Characteristics of studies included in themeta-analysis of <i>DAPK</i> promoter methylation and clinicopathological features.</p

Sensitivity analysis of <i>DAPK</i> promoter methylation and HNSCC by the random-effects method.

<p>Sensitivity analysis of <i>DAPK</i> promoter methylation and HNSCC by the random-effects method.</p

Forest plots of <i>DAPK</i> promoter methylation associated with clinicopathological features

<p>A: Forest plots of <i>DAPK</i> promoter methylation associated with sex B: Forest plots of <i>DAPK</i> promoter methylation associated with smoking status C: Forest plots of <i>DAPK</i> promoter methylation associated with alcohol status D: Forest plots of <i>DAPK</i> promoter methylation associated with lymph node invasion.</p

Characteristics of studies included in the study.

<p>Characteristics of studies included in the study.</p