Abstract
The aim of the meta-analysis was to derive a more precise assessment of the association between p16 promoter methylation and thyroid cancer risk. The PubMed, Web of Science databases and Chinese CNKI were searched for relevant articles. Ultimately, seventeen case-control studies were included with a total of 804 thyroid cancer cases and 487 controls analysis by R Software (R version 3.1.2) including meta. Crude odds ratios with 95% confidence intervals were calculated using the random-effects model which were used to assess the strength of relationship between p16 methylation and lung carcinogenesis. Funnel plots were carried out to evaluate publication bias. The meta-analysis results showed that the frequency of p16 promoter methylation in cancer tissue/blood was significantly higher than that normal tissue/ blood (OR=5.46, 95%CI 3.12-9.55, P<0.0001) by random effects model with small heterogeneity. Thus, p16 promoter methylation may be associated with thyroid cancer risk.
Highlights
Worldwide, thyroid cancer is among the less frequent malignancies
Studies included in the meta-analysis according to the inclusion criteria, 17 case–control studies were included with a total of 804 thyroid cancer cases and 487 controls (Figure 1) (Elisei et al, 1998; Schagdarsurengin et al, 2002; Boltze et al, 2003; Hoque et al, 2005; Huang et al, 2006; Nasr et al, 2006; Peng et al, 2006; Schagdarsurengin et al, 2006; Lam et al, 2007; Li and He, 2008; Wiseman et al, 2008; Dai et al, 2010; Mohammadi-asl et al, 2011; Brait et al, 2012; Dai et al, 2012; Li et al, 2013; Wang et al, 2013)
The meta-analysis results showed that the frequency of p16 promoter methylation in cancer tissue/blood was significantly higher than that normal tissue/blood (OR=5.46, 95%CI=[3.12; 9.55], z=5.94; P
Summary
Thyroid cancer is among the less frequent malignancies. in the past decades the incidence has almost doubled–attributed for the most part to the increased diagnosis of papillary thyroid cancer (Wartofsky, 2010). The p16 gene is known as a tumor suppressor gene which is may be involved in the development of thyroid cancer (Yang et al, 2012) It is localized on chromosome 9q21 and acts through the inhibition of CDK4/6 and thereby leaving the retinoblastoma (RB) protein under-phosphorylated and promoting cell cycle arrest (Ojima et al, 2006), but loss of p16 expression by its promoter methylation would lead to loss of control of the restriction point in the G1 phase of the cell cycle and favor cellular transformation (Esteller, 2008) and lead to carcinogenesis. There were many studies assessing the association between p16 promoter methylation and thyroid cancer risk, but the result is not clear. Conclusions: p16 promoter methylation may be associated with thyroid cancer risk
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