ReviewCurrent rheumatology reports2007
Genetics of ankylosing spondylitis: an update.
Review in Current rheumatology reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Association of rs11209032 and rs1004819 Polymorphisms in Interleukin-23 Receptor Gene With Ankylosing Spondylitis.Archives of rheumatology · 2016Article
- The PADI4 gene does not contribute to genetic susceptibility to rheumatoid arthritis in Chinese Han population.Rheumatology international · 2011Article
- Genetic variants of the HLA-A, HLA-B and AIF1 loci show independent associations with type 1 diabetes in Norwegian families.Genes and immunity · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substantive evidence exists that genetic factors play a pivotal role in susceptibility to ankylosing spondylitis (AS). HLA-B27 remains the most convincing and universal association of a genetic factor with AS. Over the last decade there has been immense interest in elucidating genetic variants outside the major histocompatibility complex region. Due to larger AS datasets along with recent advancements in the characterization of genetic markers and large-scale genotyping platforms, replicated non-major histocompatibility candidates have now emerged. This article reviews the current evidence regarding the genetics of AS, with an emphasis on the recent major advances, and it discusses the challenges and limitations in interpreting these studies.
Indexed as
Identifiers
17915094What 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.