Evidence map›Paper›PMID 31663908›Full record

ArticleClinical and translational gastroenterology2019

Identification of Epigenetic Methylation Signatures With Clinical Value in Crohn's Disease.

Inés Moret-Tatay, Elena Cerrillo, Esteban Sáez-González, David Hervás, Marisa Iborra, Juan Sandoval, Enrique Busó, Luis Tortosa, Pilar Nos, Belén Beltrán

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
3.0field-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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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  16. Epigenetic Regulations of AhR in the Aspect of Immunomodulation.International journal of molecular sciences · 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

10 authors at 3 institutions in 1 country.

Inés Moret-TatayInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Elena CerrilloInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Esteban Sáez-GonzálezInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
David HervásBiostatistics Unit, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Marisa IborraInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Juan SandovalBiomarkers and Precision Medicine Unit, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Enrique BusóCentral Unit for Research in Medicine (UCIM),University of Valencia, Valencia, Spain.
Luis TortosaInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Pilar NosInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Belén BeltránInflammatory Bowel Disease Research Group, Health Research Institute La Fe (IIS La Fe), Valencia, Spain.
Instituto de Investigación Sanitaria La Fe · ESLeitat Technological Center · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDNA methylation is an epigenetic mechanism that regulates gene expression and represents an important link between genotype, environment, and disease. It is a reversible and inheritable mechanism that could offer treatment targets. We aimed to assess the methylation changes on specific genes previously associated with Crohn's disease (CD) and to study their possible associations with the pathology.

methodsWe included 103 participants and grouped them into 2 cohorts (a first [n = 31] and a second validation [n = 72] cohort), with active CD (aCD) and inactive CD (iCD) and healthy participants (CTR). DNA was obtained from the peripheral blood and analyzed by the Agena platform. The selected genes were catalase (CAT), α-defensin 5 (DEFA5), FasR, FasL, tumor necrosis factor (TNF), TNFRSF1A, TNFRSF1B, PPA2, ABCB1, NOD2, PPARγ, and PKCζ. We used the elastic net algorithm and R software.

resultsWe studied 240 CpGs. Sixteen CpGs showed differential methylation profiles among aCD, iCD, and CTR. We selected for validation those with the greatest differences: DEFA5 CpG_11; CpG_13; CAT CpG_31.32; TNF CpG_4, CpG_12; and ABCB1 CpG_21. Our results validated the genes DEFA5 (methylation gain) and TNF (methylation loss) with P values < 0.001. In both cases, the methylation level was maintained and did not change with CD activity (aCD vs iCD). The subanalysis comparison between aCD and iCD showed significant differential methylation profiles in other CpGs: TNF, FAS, ABCB1, CAT, and TNFRS1BF genes. DISCUSSION: The methylation status of DEFA5 and TNF genes provides a signature biomarker that characterizes patients with CD and supports the possible implication of the environment and the immune system in CD pathogenesis.

Indexed as

AdolescentAdultalpha-DefensinsBiomarkersCase-Control StudiesCrohn DiseaseDNA MethylationEpigenesis, GeneticFemaleHumansMaleMiddle AgedRetrospective StudiesTumor Necrosis Factor-alphaYoung Adultalpha-DefensinsBiomarkersDEFA5 protein, humanTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID31663908
PMCPMC6919449
OpenAlexW2982529478

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.