Evidence map›Paper›PMID 27302879›Full record

ArticleJournal of dental research2016

Identification of Master Regulator Genes in Human Periodontitis.

A D Sawle, M Kebschull, R T Demmer, P N Papapanou

Open access · greenAbstract read
In one paragraph

Article in Journal of dental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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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 2 institutions in 2 countries.

A D SawleThe Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY, USA.
M KebschullDivision of Periodontics, Section of Oral, Diagnostic and Rehabilitation Sciences, College of Dental Medicine, Columbia University, New York, NY, USA Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany.
R T DemmerDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
P N PapapanouDivision of Periodontics, Section of Oral, Diagnostic and Rehabilitation Sciences, College of Dental Medicine, Columbia University, New York, NY, USA pp192@cumc.columbia.edu.
Columbia University · USColumbia University Irving Medical Center · US

Funding

Gene Expression in Chronic and Aggressive PeriodontitisR01DE015649 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PAPAPANOU, PANOS N · 2004 to 2006
$1.8M
Genomic approaches to the pathobiology and classification of periodontitisR03DE024735 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PAPAPANOU, PANOS N · 2015 to 2016
$480k
MicroRNA expression in gingival tissues in periodontal health and diseaseR21DE021820 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PAPAPANOU, PANOS N · 2012 to 2013
$432k
NIDCR NIH HHS R01 DE015649NIDCR NIH HHS R03 DE024735NIDCR NIH HHS R21 DE021820
6 · The paper itself

Abstract

Analytic approaches confined to fold-change comparisons of gene expression patterns between states of health and disease are unable to distinguish between primary causal disease drivers and secondary noncausal events. Genome-wide reverse engineering approaches can facilitate the identification of candidate genes that may distinguish between causal and associative interactions and may account for the emergence or maintenance of pathologic phenotypes. In this work, we used the algorithm for the reconstruction of accurate cellular networks (ARACNE) to analyze a large gene expression profile data set (313 gingival tissue samples from a cross-sectional study of 120 periodontitis patients) obtained from clinically healthy (n = 70) or periodontitis-affected (n = 243) gingival sites. The generated transcriptional regulatory network of the gingival interactome was subsequently interrogated with the master regulator inference algorithm (MARINA) and gene expression signature data from healthy and periodontitis-affected gingiva. Our analyses identified 41 consensus master regulator genes (MRs), the regulons of which comprised between 25 and 833 genes. Regulons of 7 MRs (HCLS1, ZNF823, XBP1, ZNF750, RORA, TFAP2C, and ZNF57) included >500 genes each. Gene set enrichment analysis indicated differential expression of these regulons in gingival health versus disease with a type 1 error between 2% and 0.5% and with >80% of the regulon genes in the leading edge. Ingenuity pathway analysis showed significant enrichment of 36 regulons for several pathways, while 6 regulons (those of MRs HCLS1, IKZF3, ETS1, NHLH2, POU2F2, and VAV1) were enriched for >10 pathways. Pathways related to immune system signaling and development were the ones most frequently enriched across all regulons. The unbiased analysis of genome-wide regulatory networks can enhance our understanding of the pathobiology of human periodontitis and, after appropriate validation, ultimately identify target molecules of diagnostic, prognostic, or therapeutic value.

Indexed as

AdultAlgorithmsCase-Control StudiesChronic PeriodontitisCross-Sectional StudiesGenes, RegulatorGingivaHumansPeriodontitisTranscriptomebioinformaticsgene expressiongenomicsgingivamolecular geneticsperiodontal disease(s)

Identifiers

PMID27302879
PMCPMC4959625
OpenAlexW2437270155

What OpenQuestion holds

Textmetadata
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.