ReviewNature reviews. Gastroenterology & hepatology2019
Redefining the IBDs using genome-scale molecular phenotyping.
Review in Nature reviews. Gastroenterology & hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 3 of them syntheses that pooled 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.
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.
Who cites it
59 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Transcriptome-Wide Association Study for Inflammatory Bowel Disease Reveals Novel Candidate Susceptibility Genes in Specific Colon Subsites and Tissue Categories.Journal of Crohn's & colitis · 2022Pooled it
- Risk of Urinary Bladder Cancer in Patients With Inflammatory Bowel Diseases: A Meta-Analysis.Frontiers in surgery · 2021Pooled it
- Ulcerative Colitis-Diagnostic and Therapeutic Algorithms.Deutsches Arzteblatt international · 2020Pooled it
- Concerted changes in the pediatric single-cell intestinal ecosystem before and after anti-TNF blockade.eLife · 2026Article
- Review
- Interleukin-8 in health and disease.Molecular biomedicine · 2026Review
- Reference-guided genome assembly of long non-coding rna transcripts reveals target genes associated with Crohn's disease.Scientific reports · 2026Article
- Tissue transcriptional programs stratify Crohn's disease by therapeutic response and clinical outcomes.Scientific reports · 2026Article
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- NELL-1: role and mechanisms in disease pathogenesis and development.Frontiers in cell and developmental biology · 2026Review
- Review
- MAIT Cells Maintain Intestinal Homeostasis Through IL-22 in an Experimental Colitis.Journal of inflammation research · 2026Article
- Tissue MicroRNA Expression Signatures as Diagnostic Biomarkers and Predictors of Residual Disease Activity and Relapse in Treatment-Naïve Pediatric Inflammatory Bowel Disease.Inflammatory bowel diseases · 2025Article
- IBD Prediction Is Possible, but How Far Are We from Implementing It?Inflammatory bowel diseases · 2025Review
- Reference-guided Genome Assembly of Long Non-coding RNA Transcripts Reveals Target Genes Associated With Crohn's Disease.bioRxiv : the preprint server for biology · 2025Article
- Review
- Explainable deep learning for stratified medicine in inflammatory bowel disease.Genome biology · 2025Article
- The SERPINB4 gene mutation identified in twin patients with Crohn's disease impaires the intestinal epithelial cell functions.Scientific reports · 2025Article
- Article
- Roles of zinc and zinc transporters in development, progression, and treatment of inflammatory bowel disease (IBD).Frontiers in nutrition · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The IBDs, Crohn's disease and ulcerative colitis, are chronic inflammatory conditions of the gastrointestinal tract resulting from an aberrant immune response to enteric microbiota in genetically susceptible individuals. Disease presentation and progression within and across IBDs, especially Crohn's disease, are highly heterogeneous in location, severity of inflammation and other phenotypes. Current clinical classifications fail to accurately predict disease course and response to therapies. Genome-wide association studies have identified >240 loci that confer risk of IBD, but the clinical utility of these findings remains unclear, and mechanisms by which the genetic variants contribute to disease are largely unknown. In the past 5 years, the profiling of genome-wide gene expression, epigenomic features and gut microbiota composition in intestinal tissue and faecal samples has uncovered distinct molecular signatures that define IBD subtypes, including within Crohn's disease and ulcerative colitis. In this Review, we summarize studies in both adult and paediatric patients that have identified different IBD subtypes, which in some cases have been associated with distinct clinical phenotypes. We posit that genome-scale molecular phenotyping in large cohorts holds great promise not only to further our understanding of the diverse molecular causes of IBD but also for improving clinical trial design to develop more personalized disease management and treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.