Cure8 research brief
Baseline mucosal gene-expression patterns were associated with later response to JAK inhibitors in UC, which could eventually help predict treatment benefit and illuminate relevant immune pathways.
Clinicians treating UC with JAK inhibitors, researchers studying IBD biomarkers and immune pathways, and patients considering or receiving tofacitinib or upadacitinib
This study used paired baseline and follow-up mucosal biopsies from 57 people with UC (32 on upadacitinib, 25 on tofacitinib) plus 11 healthy controls and profiled 84 genes with a targeted PCR array.
Many baseline genes and gene modules differed between later responders and non-responders, and the authors built predictive models that performed very well internally. The paper emphasizes limitations: the cohort is small and there is no external validation, so the findings are preliminary and not ready for clinical use.
The authors also found that some molecular pathways were changed by treatment even in clinical non-responders, highlighting that drug-driven pharmacodynamic effects do not always produce clinical improvement. This suggests biomarkers of pathway modulation may not equal biomarkers of benefit.
Keep the main point in mind: promising biomarker signals were reported, but they require replication in larger, independent cohorts before being used to guide care.
This is a small, single study using a targeted 84-gene panel with internal cross-validation but no external validation; results are exploratory and need replication before clinical application.
Review the original publication for the complete reporting, methods, and context.
Funding disclosed by the source: Hellenic Group for the Study of Inflammatory Bowel Disease, award 2023EOMINFEp4
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
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