Clinicopathological Significance and Potential Drug Target of CDKN2A/p16 in Endometrial Carcinoma

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.