The association of PTEN hypermethylation and breast cancer: a meta-analysis
Authors Luo S, Chen J, Mo X
Received 29 April 2016
Accepted for publication 6 July 2016
Published 12 September 2016 Volume 2016:9 Pages 5643—5650
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 4
Editor who approved publication: Professor Min Li
Shanshan Luo, Jiansi Chen, Xianwei Mo
Department of Gastrointestinal Surgery, Tumor Hospital of Guangxi Medical University, Nanning, Guangxi, People’s Republic of China
Objective: Phosphatase and tensin homolog (PTEN) deleted on chromosome 10, as a tumor suppressor gene, is crucial for the development of both familial and sporadic breast cancer (BC). The aim of this study was to perform a meta-analysis to evaluate the clinicopathological significance of PTEN promoter hypermethylation in BC.
Methods: A comprehensive literature search was made in PubMed, Embase, Google Scholar, Chinese database (China National Knowledge Infrastructure [CNKI]), and Web of Science. The analysis of pooled data was performed with Review Manager 5.2. The fixed-effects or random-effects models were used to evaluate odds ratios (ORs) and 95% confidence intervals (CIs).
Results: The meta-analysis included eight studies and a total of 923 patients. The frequency of PTEN promoter hypermethylation was significantly increased in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) compared to normal breast tissues (OR =22.53, P=0.0002 and OR =22.86, P<0.00001, respectively). However, the frequency of PTEN promoter hypermethylation was similar between IDC and DCIS. Additionally, PTEN methylation was not significantly correlated to estrogen receptor (ER) or human epidermal growth factor type 2 (HER-2) status in patients with BC.
Conclusion: PTEN promoter hypermethylation is significantly associated with the risk of DCIS and IDC, suggesting PTEN promoter hypermethylation is a valuable biomarker for diagnosis of BC.
Keywords: breast cancer, PTEN, meta-analysis, methylation, estrogen receptor, HER-2
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