Abstract
Previous studies demonstrated that the loss of function of the CDKN2A/p16/INK4A gene is mainly caused by the hypermethylation of CDKN2A, however, whether or not it is associated with the incidence and clinicopathological characteristics of endometrial carcinoma (EC) remains unclear. In this study, we conducted a meta-analysis aiming to comprehensively assess the role of CDKN2A hypermethylation in the pathogenesis of EC. A detailed literature search was made to identify the related research publications. Analysis of pooled data was performed. Odds ratio (OR) was calculated and summarized. Final analysis of 638 EC patients from 12 eligible studies was performed. The results showed that CDKN2A hypermethylation was significantly higher in EC than in normal control tissue, the pooled OR from 8 studies including 400 EC patients and 131 controls, OR = 8.39 with 95% CI 4.03–17.45, test for overall effect, Z = 5.69, P < 0.00001. Further analysis showed that CDKN2A hypermethylation was not significantly associated with tumor differentiation and clinical stage status in EC patients. The results of this meta-analysis suggest that CDKN2A hypermethylation may be implicated in the pathogenesis of EC. CDKN2A hypermethylation was not significantly associated with tumor differentiation and clinical stage status in EC patients, indicating that CDKN2A hypermethylation might be early event of EC.
Highlights
Previous studies demonstrated that the loss of function of the CDKN2A/p16/INK4A gene is mainly caused by the hypermethylation of CDKN2A, whether or not it is associated with the incidence and clinicopathological characteristics of endometrial carcinoma (EC) remains unclear
Studies meeting the following inclusion criteria were included: (1) CDKN2A methylation and/or expression which were evaluated in endometrial tissues, (2) researches which revealed the relationship between CDKN2A methylation and/or expression and endometrial cancer clinicopathological parameters and prognosis, (3) CDKN2A methylation and/or expression which were examined by methylation specific polymerase chain reaction (MSP), (4) articles which were published as a full papers in English or Chinese, (5) articles which provided sufficient information to estimate hazard ratio (HR) about overall survival and 95% confidence interval (CI) and probabilities for overall survival where applicable
The following items were collected from each study: first author, published year, geographical location, pathological status, clinical stage status and CDKN2A methylation status as well as detective methods of CDKN2A methylation (Table 1)
Summary
Previous studies demonstrated that the loss of function of the CDKN2A/p16/INK4A gene is mainly caused by the hypermethylation of CDKN2A, whether or not it is associated with the incidence and clinicopathological characteristics of endometrial carcinoma (EC) remains unclear. Further analysis showed that CDKN2A hypermethylation was not significantly associated with tumor differentiation and clinical stage status in EC patients. The results of this meta-analysis suggest that CDKN2A hypermethylation may be implicated in the pathogenesis of EC. The reported methylation rates of CDKN2A in EC are remarkably diverse We performed this meta-analysis to investigate the effects of CDKN2A hypermethylation on the incidence and major clinicopathological features of EC
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