Evidence map›Paper›PMID 40064933›Full record

ArticleScientific reports2025

Relating the molecular phenotype of ulcerative colitis to the clinical course.

Katelynn S Madill-Thomsen, Jeffery M Venner, Denise E Parsons, Konrad S Famulski, Aducio L Thiesen, Sami Hoque, Karen I Kroeker, Karen Wong, Farhad Peerani, Levinus A Dieleman and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

14 authors.

Katelynn S Madill-Thomsen *Department of Medicine, University of Alberta, Edmonton, AB, Canada.
Jeffery M Venner *Alberta Transplant Applied Genomics Center, University of Alberta, Edmonton, AB, Canada.
Denise E ParsonsDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Konrad S FamulskiDepartment of Medicine, University of Alberta, Edmonton, AB, Canada.
Aducio L ThiesenDepartment of Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada.
Sami HoqueDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Karen I KroekerDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Karen WongDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Farhad PeeraniDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Levinus A DielemanDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Frank HoentjenDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Daniel C BaumgartDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada.
Philip F HalloranDepartment of Medicine, University of Alberta, Edmonton, AB, Canada.
Brendan P HalloranDepartment of Medicine, Division of Gastroenterology, University of Alberta, 8540 - 112 Street NW, Edmonton, AB, T6G 2X8, Canada. brendan@ualberta.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expanding portfolio of targeted therapies for ulcerative colitis (UC) suggests that a more precise approach to defining disease activity will aid clinical decision-making. This prospective study used genome-wide microarrays to characterize gene expression in biopsies from the most inflamed colon segments from patients with UC and analyzed associations between molecular changes and short-term outcomes while on standard-of-care treatment. We analyzed 141 biopsies-128 biopsies from 112 UC patients and 13 biopsies from eight inflammatory bowel disease unclassified (IBDU) patients. Endoscopic disease was associated with expression of innate immunity transcripts, e.g. complement factor B (CFB); inflammasome genes (ZBP1 and PIM2); calprotectin (S100A8 and S100A9); and inflammation-, injury-, and innate immunity-associated pathway analysis terms. A cross-validated molecular machine learning classifier trained on the endoscopic Mayo subscore predicted the endoscopic Mayo subscore with area-under-the-curve of 0.85. A molecular calprotectin transcript score showed strong associations with fecal calprotectin and the endoscopic Mayo subscore. Logistic regression models showed that molecular features (e.g. molecular classifier and molecular calprotectin scores) improved the prediction of disease progression over conventional, clinical features alone (e.g. total Mayo score, fecal calprotectin, physician global assessment). The molecular features of UC showed strong correlations with disease activity and permitted development of machine-learning predictive disease classifiers that can be applied to expanded testing in diverse cohorts.

Indexed as

Colitis, UlcerativeAdultBiopsyDisease ProgressionFemaleGene Expression ProfilingHumansImmunity, InnateLeukocyte L1 Antigen ComplexMaleMiddle AgedPhenotypeProspective StudiesLeukocyte L1 Antigen ComplexDisease activityInflammatory bowel diseaseMachine learningMolecular classifierMolecular landscape

Identifiers

PMID40064933
PMCPMC11894109

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.