Evidence map›Paper›PMID 27066764›Full record

ArticleScientific reports2016

Transcriptome Variability in Keratocystic Odontogenic Tumor Suggests Distinct Molecular Subtypes.

Shijia Hu, Kimon Divaris, Joel Parker, Ricardo Padilla, Valerie Murrah, John Timothy Wright

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 17% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Amelogenin is a Potential Biomarker for the Aggressiveness in Odontogenic TumorsAsian Pacific journal of cancer prevention : APJCP · 2018
    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

6 authors at 2 institutions in 2 countries.

Shijia HuPediatric Dentistry, University of North Carolina, Chapel Hill, NC, USA.
Kimon DivarisPediatric Dentistry, University of North Carolina, Chapel Hill, NC, USA.
Joel ParkerCancer Genetics, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.
Ricardo PadillaDiagnostic Sciences, School of Dentistry, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.
Valerie MurrahDiagnostic Sciences, School of Dentistry, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.
John Timothy WrightPediatric Dentistry, University of North Carolina, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · USNational University of Singapore · SG

Funding

Phenotype and Gene Expression in Odontogenic TumorsR01DE016079 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WRIGHT, JOHN T. · 2006 to 2010
$1.5M
NIDCR NIH HHS DE016079NIDCR NIH HHS R01 DE016079
6 · The paper itself

Abstract

Keratocystic Odontogenic Tumor (KCOT) is a locally aggressive developmental cystic neoplasm thought to arise from the odontogenic epithelium. A high recurrence rate of up to 30% has been found following conservative treatment. Aggressive tumor resection can lead to the need for extensive reconstructive surgery, resulting in significant morbidity and impacting quality of life. Most research has focused on candidate-genes with a handful of studies employing whole transcriptome approaches. There is also the question of which reference tissue is most biologically-relevant. This study characterizes the transcriptome of KCOT using whole genome microarray and compare it with gene expression of different odontogenic tissues ("dentome"). Laser capture microdissection was used to isolate the neoplastic epithelial tissue in 20 cases. KCOT gene expression was compared with the "dentome" and relevant pathways were examined. Cluster analysis revealed 2 distinct molecular subtypes of KCOT. Several inflammatory pathways were activated in both subtypes. The AKT pathway was activated in one subtype while MAP kinase pathway was activated in the other. Additionally, PTCH1 expression was downregulated in both clusters suggesting involvement in KCOT tumorigenesis. In conclusion, this study provides new insights into the transcriptome of KCOT and highlights pathways that could be of diagnostic and prognostic value.

Indexed as

TranscriptomeCluster AnalysisEpitheliumGenotypeHistocytochemistryHumansLaser Capture MicrodissectionMicroarray AnalysisMicroscopyOdontogenic Tumors

Identifiers

PMID27066764
PMCPMC4828651
OpenAlexW2340486819

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.