ArticleGenes and immunity2012
Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls.
Article in Genes and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed.
- Identification of systemic biomarkers and potential drug targets for age-related macular degeneration.Frontiers in aging neuroscience · 2024Article
- Copy number variation of CCL3L1 among three major ethnic groups in Malaysia.BMC genetics · 2020Article
- Population-wide copy number variation calling using variant call format files from 6,898 individuals.Genetic epidemiology · 2020Article
- Characterization of copy number variants for CCL3L1 gene in rheumatoid arthritis for French trio families and Tunisian cases and controls.Clinical rheumatology · 2016Article
- SRBreak: A Read-Depth and Split-Read Framework to Identify Breakpoints of Different Events Inside Simple Copy-Number Variable Regions.Frontiers in genetics · 2016Article
- Complex and multi-allelic copy number variation in human disease.Briefings in functional genomics · 2015Review
- Human gene copy number variation and infectious disease.Human genetics · 2014Review
- Rapid and accurate large-scale genotyping of duplicated genes and discovery of interlocus gene conversions.Nature methods · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 (CCL3L1) and its contribution to rheumatoid arthritis (RA) susceptibility. In order to draw robust conclusions about CCL3L1 involvement in RA, we have performed association analysis (CNVtools) using genotyping by the paralogue ratio test of a Norwegian RA case-control material (N=1877). We also analyzed the associations after stratification for anti-citrullinated peptide antibody (ACPA) status. Clear clusters representing specific copy number classes were evident, but significant differential bias was observed resulting in a systematic trend toward slightly higher apparent copy number for cases relative to controls. Controlling for bias revealed no significant differences in copy number distribution either between all patients and controls, or after ACPA stratification. Our results do not support involvement of the CCL3L1 CNV in RA susceptibility.
Indexed as
Identifiers
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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.