SynthesisTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Promoter methylation and polymorphism of E-cadherin gene may confer a risk to prostate cancer: a meta-analysis based on 22 studies.
Synthesis in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The clinicopathological significance and potential drug target of E-cadherin in NSCLC.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- Differences in E-Cadherin and Syndecan-1 Expression in Different Types of Ameloblastomas.Analytical cellular pathology (Amsterdam) · 2018Article
- Impact of Candidate Genetic Polymorphisms in Prostate Cancer: An Overview.Molecular diagnosis & therapy · 2016Review
- Article
- The MIF -173G/C gene polymorphism increase gastrointestinal cancer and hematological malignancy risk: evidence from a meta-analysis and FPRP test.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has suggested that -160C/A polymorphism and promoter methylation of E-cadherin gene may contribute to the risk of prostate cancer. However, the results are still conflicting. We aim to systematically evaluate the potential of promoter methylation and polymorphism in E-cadherin gene to confer a risk to prostate cancer through meta-analysis. PubMed, Embase, Web of Science, Cochrane Library, and Chinese National Knowledge Infrastructure (CNKI) databases were searched to identify eligible studies published before April 1, 2014. Pooled odds ratios (ORs) with their 95 % confidence intervals (95 % CIs) were calculated by using the random-effect model or the fixed-effect model, according to heterogeneity test. Subgroup analyses were also performed to explore the potential sources of heterogeneity. Sensitivity and publication bias analyses were used to test the robustness of our results. We performed a meta-analysis of 22 included studies, with 11 on -160C/A polymorphism and another 11 on promoter methylation of E-cadherin gene. Our meta-analysis results suggested that E-cadherin -160C/A polymorphism may be a potential risk factor for prostate cancer. Furthermore, we observed that the frequencies of promoter methylation of E-cadherin gene in the prostate cancer tissues were significantly higher than those of normal tissues, indicating that promoter methylation of E-cadherin gene may play an important role in prostate carcinogenesis. In conclusion, the present meta-analysis provides further evidence that promoter methylation and -160C/A polymorphism of E-cadherin gene may confer a risk to prostate cancer. Identifying these risk factors for prostate cancer will improve early detection, allow for selective chemoprevention, and provide further insights into its disease mechanisms.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.