Trial reportGenes and immunity2003
Pharmacogenomic analysis of interferon receptor polymorphisms in multiple sclerosis.
Trial report in Genes and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 78 citations in OpenAlex.
- IFN-Induced Protein with Tetratricopeptide Repeats 2 Limits Autoimmune Inflammation by Regulating Myeloid Cell Activation and Metabolic Activity.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Pharmacogenetic Predictors of Response to Interferon Beta Therapy in Multiple Sclerosis.Molecular neurobiology · 2021Article
- Association study of promoter polymorphisms of interferon alpha and beta receptor subunit 1 (IFNAR1) gene and therapeutic response to interferon-beta in patients with multiple sclerosis.Molecular biology reports · 2021Article
- Pharmacogenomics of Multiple Sclerosis: A Systematic Review.Frontiers in neurology · 2019Review
- Pharmacogenetic Biomarkers to Predict Treatment Response in Multiple Sclerosis: Current and Future Perspectives.Multiple sclerosis international · 2017Review
- Candidate gene study of TRAIL and TRAIL receptors: association with response to interferon beta therapy in multiple sclerosis patients.PloS one · 2013Article
- Pharmacogenomic update on multiple sclerosis: a focus on actual and new therapeutic strategies.The pharmacogenomics journal · 2012Review
- Determinants of interferon β efficacy in patients with multiple sclerosis.Nature reviews. Neurology · 2011Review
- Predicting responders to therapies for multiple sclerosis.Nature reviews. Neurology · 2009Review
- Genetic polymorphisms, their allele combinations and IFN-beta treatment response in Irish multiple sclerosis patients.Pharmacogenomics · 2009Article
- Multiple sclerosis genetics: leaving no stone unturned.Genes and immunity · 2005Review
- Transcription-based prediction of response to IFNbeta using supervised computational methods.PLoS biology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system characterized by progressive neurological dysfunction. No curative therapy is currently available, and approximately 80-90% of afflicted individuals are ultimately disabled. Interferon beta (IFNbeta) has been shown to decrease clinical relapses, reduce brain disease activity, and possibly slow progression of disability. However, the overall effect of treatment is partial and a substantial number of patients are considered poor or nonresponders. For this report, we tested the pharmacogenomic effects of eight polymorphisms in the interferon receptor genes (IFNAR1 and IFNAR2) in a group of 147 patients undergoing open-label IFNbeta therapy. Overall, no significant differences in the distribution of responders and nonresponders, classified based on prospectively acquired primary and secondary clinical end points, were observed when stratified by any of the studied IFNAR gene polymorphisms. A trend detected with a single nucleotide polymorphism SNP 16469 (A/T) located at the third intron of the IFNAR1 gene, suggesting modest association with relapse-free status, will require confirmation in an independent data set. In addition, no significant association was observed of any of the IFNAR gene polymorphisms with susceptibility to MS, as studied by a family-based association analysis.
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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.