Evidence map›Paper›PMID 24971029›Full record

ReviewThe application of clinical genetics2014

The genetic basis of ankylosing spondylitis: new insights into disease pathogenesis.

Florence Wl Tsui, Hing Wo Tsui, Ali Akram, Nigil Haroon, Robert D Inman

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The application of clinical genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
10.7field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

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  16. Association of IFN-γ polymorphisms with ankylosing spondylitis risk.Journal of cellular and molecular medicine · 2020
    Article
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  19. Relationship of CARD8 Gene Polymorphisms with Susceptibility to Ankylosing Spondylitis: A Case-Control Study.Medical science monitor : international medical journal of experimental and clinical research · 2020
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  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 2 countries.

Florence Wl TsuiGenetics and Development Division, Toronto Western Research Institute, University Health Network ; Department of Immunology.
Hing Wo TsuiGenetics and Development Division, Toronto Western Research Institute, University Health Network.
Ali AkramGenetics and Development Division, Toronto Western Research Institute, University Health Network ; Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
Nigil HaroonGenetics and Development Division, Toronto Western Research Institute, University Health Network ; Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
Robert D InmanGenetics and Development Division, Toronto Western Research Institute, University Health Network ; Institute of Medical Science, University of Toronto, Toronto, ON, Canada.
University Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankylosing spondylitis (AS) is a complex disease involving multiple risk factors, both genetic and environmental. AS patients are predominantly young men, and the disease is characterized by inflammation and ankylosis, mainly at the cartilage-bone interface and enthesis. HLA-B27 has been known to be the major AS-susceptibility gene for more than 40 years. Despite advances made in the past few years, progress in the search for non-human leukocyte antigen susceptibility genes has been hampered by the heterogeneity of the disease. Compared to other complex diseases, such as inflammatory bowel disease (IBD), fewer susceptibility loci have been identified in AS. Furthermore, non-major histocompatibility-complex susceptibility loci discovered, such as ERAP1 and IL23R, are likely contributors to joint inflammation. Identification and confirmation of functional variants remains a significant challenge of investigations involving genome-wide association studies (GWAS). It remains unclear why none of the AS-susceptibility genes identified in GWAS appear to be directly involved in the ankylosing process. Numerous reviews have recently been published on the genetics of AS. Therefore, aside from a brief summary of what AS GWAS has successfully achieved thus far, this review will focus on directions that could address unanswered questions raised by GWAS.

Indexed as

ankylosing spondylitisankylosisclinical subsetsgenome-wide association studiesjoint and gut inflammationrisk loci

Identifiers

PMID24971029
PMCPMC4070859
OpenAlexW1969833817

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.