Title of article :
Frequent loss expression of dab2 and promotor hypermethylation in human cancers: A meta-analysis and systematic review
Author/Authors :
Zhang, Ziyin Meishan City People’s Hospital - Department of Neurosurgery, China , Chen, Yihua People’s Liberation Army General Hospital of Chengdu Military Region - Department of Pathology, China , Tang, JianJian Meishan City People’s Hospital - Department of Neurosurgery, China , Xie, Xuemei People’s Liberation Army General Hospital of Chengdu Military Region - Department of Pathology, China
From page :
432
To page :
437
Abstract :
Objective: Disabled-2 (Dab2) is an important endocytic adaptor which plays an inhibition role in cancer cell growth. The objective of this study was to systematically review expressions of Dab2 in human cancers. Methods: Eligible studies about Dab2 in human cancers were retrieved from databases of PubMed, Embase, Web of Science. Odds Ratios (ORs) with 95% confidence intervals (CIs) were calculated using Review Manager 5.0 software and statistical analyses were performed by the SPSS 13.0 software. Results: Fourteen case-control studies with a total of 689 human tumor tissues, 332 control tissues and 32 cancer cell lines were included in the meta-analysis study. The results indicated loss expressions of Dab2 were observed in 74.9% and 46.9% in human malignant cancer tissues and cancer cell lines, respectively. The ratio of Dab2 promotor hypermethylation is 34.54% in cancer tissues which Dab2 expression are lost, but none in the control tissues or cells by Methylation-specific PCR (MSP). Conclusions: The expressions of Dab2 are frequently lost in human malignant cancer tissues, and promotor hypermethylation of Dab2 are common in human malignant cancer tissues, which is an important factor for the loss expression of Dab2 in human cancers tissues.
Keywords :
Dab2 , Expression , Human , Cancers , Meta , Analysis
Journal title :
Pakistan Journal of Medical Sciences
Journal title :
Pakistan Journal of Medical Sciences
Record number :
2563860
Link To Document :
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