Evidence map›Paper›PMID 29040430›Full record

ArticleJournal of Crohn's & colitis2018

Transcriptomic Landscape of Treatment-Naïve Ulcerative Colitis.

Hagar Taman, Christopher G Fenton, Inga V Hensel, Endre Anderssen, Jon Florholmen, Ruth H Paulssen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 3 pooled it
5.3field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 87 citations in OpenAlex.

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  19. Mechanisms and regulation of defensins in host defense.Signal transduction and targeted therapy · 2023
    Review
  20. Methylation-Regulated Long Non-Coding RNA Expression in Ulcerative Colitis.International journal of molecular sciences · 2023
    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.

Hagar TamanGenomic Support Centre Tromsø [GSCT], Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
Christopher G FentonGenomic Support Centre Tromsø [GSCT], Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
Inga V HenselGenomic Support Centre Tromsø [GSCT], Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
Endre AnderssenGenomic Support Centre Tromsø [GSCT], Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
Jon FlorholmenGastroenterology and Nutrition Research Group, Department of Clinical Medicine, UiT-The Artic University of Norway, Tromsø, Norway.
Ruth H PaulssenGenomic Support Centre Tromsø [GSCT], Department of Clinical Medicine, UiT-The Arctic University of Norway, Tromsø, Norway.
UiT The Arctic University of Norway · NOUniversity Hospital of North Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsUlcerative colitis [UC] is a chronic inflammatory disease that effects the gastrointestinal tract and is considered one of the most prominent and common forms of inflammatory bowel disease [IBD]. This study aimed to define and describe the entire transcriptomic landscape in a well-stratified, treatment-naïve UC patient population compared with control patients by using next-generation technology, RNA-Seq.

methodsMucosal biopsies from treatment-naïve UC patients [n = 14], and healthy controls [n = 16] underwent RNA-Seq. Principal component analysis [PCA], cell deconvolution methods, and diverse statistical methods were applied to obtain and characterise a dataset of significantly differentially expressed genes [DEGs].

resultsAnalyses revealed 1480 significantly DEGs in treatment-naïve UC when compared with controls. Cell populations of monocytes, T cells, neutrophils, B cells/ lymphoid cells, and myeloid cells were increased during inflammation, whereas the fraction of epithelial cells were reduced in UC, which is reflected by the DEGs; 79 DEGs were identified as IBD susceptibility genes, and 58 DEGs were expressed in a gender-specific manner. MUC5B, REG3A, DEFA5, and IL33 might be considered as colorectal cancer [CRC] risk factors following UC in males. AQP9 together with CLDN2 may have a role regulating tissue-specific physiological properties in tight junctions in UC. An additional functional role for AQP9 in the synthesis and/or the function of mucus can be implied.

conclusionsThis study reveals new potential players in UC pathogenesis in general, and provides evidence for a gender-dependent pathogenesis for UC. These results can be useful for the development of personalised treatment strategies for UC in the future.

Indexed as

TranscriptomeAdultAgedalpha-DefensinsAquaporinsBiopsyCase-Control StudiesClaudinsColitis, UlcerativeColon, SigmoidColorectal NeoplasmsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingHumansalpha-DefensinsAQP9 protein, humanAquaporinsClaudinsCLDN2 protein, humanDEFA5 protein, humanIL33 protein, humanInterleukin-33MUC5B protein, humanMucin-5BPancreatitis-Associated ProteinsREG3A protein, human

Identifiers

PMID29040430
PMCPMC6290885
OpenAlexW2762036315

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.