ArticleFrontiers in genetics2026
Exploratory transcriptomic analysis suggests candidate genes associated with loss of response to ustekinumab in Crohn's disease.
Article in Frontiers in genetics, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Despite the favorable safety and efficacy of ustekinumab in clinical practice for Crohn's disease, a subset of Crohn's disease patients still experience loss of response to this treatment. This study was thus conducted to investigate the differential gene expression underlying ustekinumab loss of response in Crohn's disease patients. Methods: This prospective study, grouped by response to ustekinumab, collected peripheral blood mononuclear cells from refractory moderate-to-severe adult Crohn's disease patients (8 vs. 9) who were admitted to the Second Affiliated Hospital of Guangzhou Medical University and received initial ustekinumab treatment between January 2024 and June 2025 for RNA sequencing. For exploratory pathway analysis, differentially expressed genes identified by DESeq2 using exploratory thresholds (|FC| > 1.5, Results: RNA sequencing identified 510 differentially expressed genes between ustekinumab responders and non-responders. Trait association analysis showed that the cyan module was the module most strongly associated with both ustekinumab non-response and stricturing behavior, consistent with the independent influence of stricturing behavior identified in the retrospective clinical study. This module was enriched in platelet activation, neutrophil extracellular trap formation, and focal adhesion (KEGG), as well as coagulation and platelet aggregation (GO). Among the 10 candidate genes selected for validation, FFAR2, ITGA2B, SOCS3, and KCNJ15 exhibited statistically significant differential expression. Conclusion: Our findings suggest that loss of response may be potentially associated with pro-inflammatory pathways independent of the drug's action pathways, as well as a "pro-fibrotic immune microenvironment" linked to intestinal strictures. Additionally, preliminary validation indicated that FFAR2, ITGA2B, SOCS3, and KCNJ15 may provide new perspectives for candidate differentially expressed genes associated with ustekinumab loss of response.
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.