ArticleLife (Basel, Switzerland)2023
Identification of Specific Biomarkers and Pathways in the Treatment Response of Infliximab for Inflammatory Bowel Disease: In-Silico Analysis.
Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- SEMA3B is associated with disease activity and infliximab response in IBD patients but does not contribute to the development of intestinal inflammationFrontiers in immunology · 2026Article
- Comprehensive computational strategies for multi-target drug discovery in inflammatory bowel disease utilizing bioactive compounds.Scientific reports · 2025Article
- Surgeons Knowledge, Attitude, and Practice Toward Preoperative Inflammatory Bowel Disease Medications and Post-Operative Complications.Therapeutics and clinical risk management · 2025Article
- Post-operative Crohn's Disease Recurrence and Infectious Complications: A Transcriptomic Analysis.Digestive diseases and sciences · 2025Article
- Exploring Microbial Metabolite Receptors in Inflammatory Bowel Disease: An In Silico Analysis of Their Potential Role in Inflammation and Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Predictive, preventive and personalised approach as a conceptual and technological innovation in primary and secondary care of inflammatory bowel disease benefiting affected individuals and populations.The EPMA journal · 2024Review
- Aryl Hydrocarbon Receptor Regulates Muc2 Production Independently of IL-22 during Colitis.International journal of molecular sciences · 2024Article
- Exploring potential biomarkers and therapeutic targets in inflammatory bowel disease: insights from a mega-analysis approach.Frontiers in immunology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract. In biological therapy, infliximab became the first anti-tumor necrosis factor (TNF) agent approved for IBD. Despite this success, infliximab is expensive, often ineffective, and associated with adverse events. Prediction of infliximab resistance would improve overall potential outcomes. Therefore, there is a pressing need to widen the scope of investigating the role of genetics in IBD to their association with therapy response.
methodsIn the current study, an in-silico analysis of publicly available IBD patient transcriptomics datasets from Gene Expression Omnibus (GEO) are used to identify subsets of differentially expressed genes (DEGs) involved in the pathogenesis of IBD and may serve as potential biomarkers for Infliximab response. Five datasets were found that met the inclusion criteria. The DEGs for datasets were identified using limma R packages through the GEOR2 tool. The probes' annotated genes in each dataset intersected with DGEs from all other datasets. Enriched gene Ontology Clustering for the identified genes was performed using Metascape to explore the possible connections or interactions between the genes.
results174 DEGs between IBD and healthy controls were found from analyzing two datasets (GSE14580 and GSE73661), indicating a possible role in the pathogenesis of IBD. Of the 174 DEGs, five genes (SELE, TREM1, AQP9, FPR2, and HCAR3) were shared between all five datasets. Moreover, these five genes were identified as downregulated in the infliximab responder group compared to the non-responder group.
conclusionsWe hypothesize that alteration in the expression of these genes leads to an impaired response to infliximab in IBD patients. Thus, these genes can serve as potential biomarkers for the early detection of compromised infliximab response in IBD patients.
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