ReviewGenes and immunity2005
Multiple sclerosis genetics: leaving no stone unturned.
Review in Genes and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.
- Evidence for CRHR1 in multiple sclerosis using supervised machine learning and meta-analysis in 12,566 individuals.Human molecular genetics · 2010Pooled it
- Mapping candidate non-MHC susceptibility regions to multiple sclerosis.Genes and immunity · 2006Pooled it
- Trial
- Imprinting methylation predicts hippocampal volumes and hyperintensities and the change with age in later life.Scientific reports · 2021Article
- Relationship between miR-155 and miR-146a polymorphisms and susceptibility to multiple sclerosis in an Egyptian cohort.Biomedical reports · 2020Article
- Several household chemical exposures are associated with pediatric-onset multiple sclerosis.Annals of clinical and translational neurology · 2018Article
- Exome sequencing study in patients with multiple sclerosis reveals variants associated with disease course.Journal of neuroinflammation · 2018Article
- A non-synonymous single-nucleotide polymorphism associated with multiple sclerosis risk affects the EVI5 interactome.Human molecular genetics · 2015Article
- Annotation of functional variation within non-MHC MS susceptibility loci through bioinformatics analysis.Genes and immunity · 2014Article
- The association of -330 interleukin-2 gene polymorphism with its plasma concentration in Iranian multiple sclerosis patients.Scientifica · 2014Article
- The association of -475 and -631 interleukin-2 gene polymorphism with multiple sclerosis in Iranian patients.Cell journal · 2013Article
- High-throughput, high-fidelity HLA genotyping with deep sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Gene expression profiling in multiple sclerosis brain.Neurobiology of disease · 2012Review
- Polymorphism of Apo lipoprotein E gene and the risk of multiple sclerosis.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2011Article
- Genome-wide association study of severity in multiple sclerosis.Genes and immunity · 2011Article
- Incidence of acquired CNS demyelinating syndromes in a multiethnic cohort of children.Neurology · 2011Article
- Article
- Human endogenous retroviruses and multiple sclerosis: innocent bystanders or disease determinants?Biochimica et biophysica acta · 2011Review
- Variation within DNA repair pathway genes and risk of multiple sclerosis.American journal of epidemiology · 2010Article
- An application of Random Forests to a genome-wide association dataset: methodological considerations & new findings.BMC genetics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Compelling epidemiologic and molecular data indicate that genes play a primary role in determining who is at risk for developing multiple sclerosis (MS), how the disease progresses, and how someone responds to therapy. The genetic component of MS etiology is believed to result from the action of allelic variants in several genes. Their incomplete penetrance and moderate individual effect probably reflects epistatic interactions, post-transcriptional regulatory mechanisms, and significant environmental influences. Equally significant, it is also likely that locus heterogeneity exists, whereby specific genes influence susceptibility and pathogenesis in some individuals but not in others. With the aid of novel analytical algorithms, the combined study of genomic, transcriptional, proteomic, and phenotypic information in well-controlled study groups will define a useful conceptual model of pathogenesis and a framework for understanding the mechanisms of action of existing therapies for this disorder, as well as the rationale for novel curative strategies.
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.