Evidence map›Paper›PMID 25887408›Full record

ArticleBMC genomics2015

Genome-wide expression analysis suggests a crucial role of dysregulation of matrix metalloproteinases pathway in undifferentiated thyroid carcinoma.

Jesús Espinal-Enríquez, Said Muñoz-Montero, Ivan Imaz-Rosshandler, Aldo Huerta-Verde, Carmen Mejía, Enrique Hernández-Lemus

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Loss of long-range co-expression is a common feature in cancer.NPJ systems biology and applications · 2026
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  13. The Emerging Role of Adhesion GPCRs in Cancer.ACS pharmacology & translational science · 2020
    Review
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  18. Cell Cycle M-Phase Genes Are Highly Upregulated in Anaplastic Thyroid Carcinoma.Thyroid : official journal of the American Thyroid Association · 2017
    Article
  19. 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 1 country.

Jesús Espinal-EnríquezNational Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610, México. jespinal@inmegen.gob.mx.
Said Muñoz-MonteroNational Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610, México. smunoz@grupoabraxas.com.
Ivan Imaz-RosshandlerNational Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610, México. iimaz@inmegen.gob.mx.
Aldo Huerta-VerdeNational Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610, México. ajosuehv@gmail.com.
Carmen MejíaFaculty of Natural Sciences, Autonomous University of Querétaro, P.O. Box 184, Querétaro, 76230, México. Maria.C.Mejia@uv.es.
Enrique Hernández-LemusNational Institute of Genomic Medicine, Periférico Sur 4809, Arenal Tepepan, TlalpanMéxico City, 14610, México. ehernandez@inmegen.gob.mx.
National Institute of Genomic Medicine · MXAutonomous University of Queretaro · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThyroid cancer (TC) is the most common malignant cancer of the Endocrine System. Histologically, there are three main subtypes of TC: follicular, papillary and anaplastic. Diagnosing a thyroid tumor subtype with a high level of accuracy and confidence is still a difficult task because genetic, molecular and cellular mechanisms underlying the transition from differentiated to undifferentiated thyroid tumors are not well understood. A genome-wide analysis of these three subtypes of thyroid carcinoma was carried out in order to identify significant differences in expression levels as well as enriched pathways for non-shared molecular and cellular features between subtypes.

resultsInhibition of matrix metalloproteinases pathway is a major event involved in thyroid cancer progression and its dysregulation may result crucial for invasiveness, migration and metastasis. This pathway is drastically altered in ATC while in FTC and PTC, the most important pathways are related to DNA-repair activation or cell to cell signaling events.

conclusionA progression from FTC to PTC and then to ATC was detected and validated on two independent datasets. Moreover, PTX3, COLEC12 and PDGFRA genes were found as possible candidates for biomarkers of ATC while GPR110 could be tested to distinguish PTC over other tumor subtypes. The genome-wide analysis emphasizes the preponderance of pathway-dysregulation mechanisms over simple gene-malfunction as the main mechanism involved in the development of a cancer phenotype.

Indexed as

Gene Expression Regulation, NeoplasticGenome-Wide Association StudySignal TransductionBiomarkersCell CommunicationCell SurvivalComputational BiologyDatabases, GeneticHumansMatrix MetalloproteinasesMolecular Sequence AnnotationNeoplasm GradingReproducibility of ResultsROC CurveThyroid NeoplasmsBiomarkersMatrix Metalloproteinases

Identifiers

PMID25887408
PMCPMC4377021
OpenAlexW2103860066

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.