Evidence map›Paper›PMID 27255271›Full record

ArticleBMC cancer2016

High-risk oral leukoplakia is associated with aberrant promoter methylation of multiple genes.

Masanobu Abe, Satoshi Yamashita, Yoshiyuki Mori, Takahiro Abe, Hideto Saijo, Kazuto Hoshi, Toshikazu Ushijima, Tsuyoshi Takato

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  18. Biomarkers in Tumorigenesis Using Cancer Cell Lines: A Systematic ReviewAsian Pacific journal of cancer prevention : APJCP · 2017
    Article
  19. The Clinical Signification of Claudin-11 Promoter Hypermethylation for Laryngeal Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  20. Article
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 1 country.

Masanobu AbeDepartment of Oral & Maxillofacial Surgery, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. abem-ora@h.u-tokyo.ac.jp.
Satoshi YamashitaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Yoshiyuki MoriDepartment of Dentistry, Oral & Maxillofacial Surgery, Jichi Medical University, Tochigi, Japan.
Takahiro AbeDepartment of Oral & Maxillofacial Surgery, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Hideto SaijoDepartment of Oral & Maxillofacial Surgery, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Kazuto HoshiDepartment of Oral & Maxillofacial Surgery, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Toshikazu UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Tsuyoshi TakatoDepartment of Oral & Maxillofacial Surgery, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
University of Tokyo Hospital · JPJichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEarly detection of oral squamous cell carcinomas (OSCCs) is urgently needed to improve the prognosis and quality of life (QOL) of patients. Oral leukoplakias (OLs), known as the most common premalignant lesions in the oral cavity, often precede OSCCs. Especially, OLs with dysplasia are known to have a high risk of malignant transformation. Here, we searched for the promoter methylation characteristic of high-risk OLs.

methodsTo identify methylation-silenced genes, a combined analysis of methylated DNA immunoprecipitation (MeDIP) - CpG island (CGI) microarray analysis and expression microarray analysis after treatment with a demethylating agent was performed in two OSCC cell lines (Ca9-22 and HSC-2). The methylation statuses of each gene were examined by methylation-specific PCR.

resultsA total of 52 genes were identified as candidates for methylation-silenced genes in Ca9-22 or HSC-2. The promoter regions of 13 genes among the 15 genes randomly selected for further analysis were confirmed to be methylated in one or more of five cell lines. In OSCC tissues (n = 26), 8 of the 13 genes, TSPYL5, EGFLAM, CLDN11, NKX2-3, RBP4, CMTM3, TRPC4, and MAP6, were methylated. In OL tissues (n = 24), seven of the eight genes, except for EGFLAM, were found to be methylated in their promoter regions. There were significantly greater numbers of methylated genes in OLs with dysplasia than in those without dysplasia (p < 0.0001).

conclusionsOLs at high risk for malignant transformation were associated with aberrant promoter methylation of multiple genes.

Indexed as

AdultAgedAged, 80 and overCarcinoma, Squamous CellCell Transformation, NeoplasticDNA MethylationEarly Detection of CancerFemaleGene Expression ProfilingHumansImmunoprecipitationLeukoplakia, OralMaleMiddle AgedOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionGene silencingMethylationOral leukoplakiaOral squamous cell carcinomaPromoter methylation

Identifiers

PMID27255271
PMCPMC4891845
OpenAlexW2418651968

What OpenQuestion holds

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LicenceCC BY
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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.