Evidence map›Paper›PMID 21697275›Full record

Trial reportCancer prevention research (Philadelphia, Pa.)2011

EZH2 promotes malignant phenotypes and is a predictor of oral cancer development in patients with oral leukoplakia.

Wei Cao, Rania H Younis, Jiang Li, Haiyan Chen, Ronghui Xia, Li Mao, Wantao Chen, Hening Ren

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  18. OncoTargets and therapy · 2020
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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

8 authors at 2 institutions in 2 countries.

Wei CaoDepartment of Oral and Maxillofacial Surgery, Ninth People's Hospital, School of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai, China.
Rania H Younis
Jiang Li
Haiyan Chen
Ronghui Xia
Li Mao
Wantao Chen
Hening Ren
Shanghai Jiao Tong University · CNUniversity of Maryland, Baltimore · US

Funding

TRAINING IN OROFACIAL BIOLOGY AND NEUROSCIENCET32DE007309 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI GORDON, SHARON M. · 1997 to 2012
$6.8M
NIDCR NIH HHS T32 DE007309NIDCR NIH HHS T32 DE007309-12
6 · The paper itself

Abstract

Oral leukoplakia (OL) is the most common premalignancy in the oral cavity. A small proportion of OLs progresses to oral squamous cell carcinoma (OSCC). To assess OSCC risk of OLs, we investigated the role of the transcriptional repressor enhancer of zeste homolog 2 (EZH2) in oral tumorigenesis and its clinical implication as an OSCC risk predictor. Immunohistochemistry was used to measure EZH2 expression in OLs from 76 patients, including 37 who later developed OSCC and 39 who did not. EZH2 expression was associated with clinicopathologic parameters and clinical outcomes. To determine the biological role of EZH2 in OL, EZH2 level was reduced using EZH2 siRNAs in Leuk-1 cells, its impact on cell cycle, anchorage-dependent/independent growth, and invasion was assessed. We observed strong EZH2 expression in 34 (45%), moderate expression in 26 (34%), and weak/no expression in 16 (21%) of the OLs. The higher EZH2 levels were strongly associated with dysplasia (P < 0.001) and OSCC development (P < 0.0001). Multivariate analysis indicated that EZH2 expression was the only independent factor for OSCC development (P < 0.0001). At 5 years after diagnosis, 80% of patients whose OLs expressed strong EZH2 developed OSCC whereas only 24% patients with moderate and none with weak/no EZH2 expression did so (P < 0.0001). In Leuk-1 cells, EZH2 downregulation resulted in G(1) arrest; decreased invasion capability, decreased anchorage-independent growth; downregulation of cyclin D1 and upregulation of p15(INK4B). Our data suggest that EZH2 plays an important role in OL malignant transformation and may be a biomarker in predicting OSCC development in patients with OLs.

Indexed as

AdultAgedBlotting, WesternCarcinoma, Squamous CellCell AdhesionCell CycleCell Line, TumorCell MovementCell ProliferationCohort StudiesDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanPolycomb Repressive Complex 2RNA, Small InterferingTranscription Factors

Identifiers

PMID21697275
PMCPMC3677701
OpenAlexW2171449084

What OpenQuestion holds

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Registered trials

None linked

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.