ArticleScientific reports2026
Tissue transcriptional programs stratify Crohn's disease by therapeutic response and clinical outcomes.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Crohn's disease is biologically heterogeneous, and current clinical classifications poorly predict treatment response or disease progression. The molecular programs that drive clinical outcomes in Crohn's disease remain poorly defined. We generated and analyzed whole-transcriptome RNA-sequencing data from non-inflamed colonic biopsies of 101 well-characterized Crohn's disease patients. We performed weighted gene co-expression network analysis and identified 15 transcriptional programs that stratified Crohn's disease independent of conventional clinical classification. We then tested associations between these programs and clinical outcomes, including primary and secondary treatment failure, surgical burden, and perianal disease. A neutrophil activation program enriched for CD69 expression was strongly associated with both primary and secondary treatment failure, identifying a mucosal immune phenotype of therapeutic resistance. A fibro-proliferative program centered on SERPINE1 expression correlated with higher cumulative surgical burden, implicating tissue remodeling pathways in progressive disease. We also discovered an antimicrobial program, marked by elevated DEFA5 and DEFA6, in colonic mucosa; this signature was enriched in patients with treatment failure and validated by DEFA5 immunofluorescence. A distinct program uniquely associated with perianal disease highlights the molecular features of this severe phenotype that are not captured by standard clinical metrics. In conclusion, colonic transcriptional programs identify biologically meaningful disease states in Crohn's disease that associate with treatment failure, surgical risk, and perianal involvement. These findings provide a molecular basis for prognostic biomarkers and targeted therapeutic stratification in Crohn's disease.
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.