Evidence map›Paper›PMID 26283007›Full record

SynthesisScientific reports2015

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

Li Su, Hanwei Wang, Jingwei Miao, Ying Liang

Open access · goldAbstract readMeta-AnalysisReview
In one paragraph

Synthesis in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  12. Silencing of TRB3 Ameliorates Diabetic Tubule Interstitial Nephropathy via PI3K/AKT Signaling in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2017
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 1 country.

Li SuDepartment of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100006, China.
Hanwei WangNanjing Normal University, Nanjing 210097.
Jingwei MiaoDepartment of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100006, China.
Ying LiangNanjing University, Nanjing 210023.
Beijing Obstetrics and Gynecology Hospital · CNCapital Medical University · CNNanjing Normal University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Biomarkers, TumorCyclin-Dependent Kinase Inhibitor p16Endometrial NeoplasmsFemaleGenetic MarkersGenetic Predisposition to DiseaseHumansNeoplasm ProteinsPolymorphism, Single NucleotidePrevalenceRisk FactorsBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16Genetic MarkersNeoplasm Proteins

Identifiers

PMID26283007
PMCPMC4642515
OpenAlexW2412848062

What OpenQuestion holds

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Registered trials

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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.