ArticlePLoS genetics2010
Allelic variation at the 8q23.3 colorectal cancer risk locus functions as a cis-acting regulator of EIF3H.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 5 of them syntheses that pooled it.
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.
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Who cites it
51 citing papers in PubMed, 5 syntheses or guidelines pooled it, 82 citations in OpenAlex.
- The landscape of GWAS validation; systematic review identifying 309 validated non-coding variants across 130 human diseases.BMC medical genomics · 2022Pooled it
- Pooled it
- The association of low penetrance genetic risk modifiers with colorectal cancer in lynch syndrome patients: a systematic review and meta-analysis.Familial cancer · 2018Pooled it
- Quantitative assessment of the influence of common variation rs16892766 at 8q23.3 with colorectal adenoma and cancer susceptibility.Molecular genetics and genomics : MGG · 2015Pooled it
- Analyzing large-scale samples confirms the association between rs16892766 polymorphism and colorectal cancer susceptibility.Scientific reports · 2015Pooled it
- Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.PloS one · 2014Trial
- Polymorphisms in the ERCC5 gene and risk of esophageal squamous cell carcinoma (ESCC) in Eastern Chinese populations.PloS one · 2012Trial
- AC005034.3/hsa-miR-126-5p/EIF3H axis: bioinformatics analysis, expression validation, and association with prognosis and immunosuppressive microenvironment in pancreatic adenocarcinoma.Frontiers in cell and developmental biology · 2026Article
- X-ray cross-complementing family: the bridge linking DNA damage repair and cancer.Journal of translational medicine · 2023Review
- Evidence for shared genetic risk factors between lymphangioleiomyomatosis and pulmonary function.ERJ open research · 2022Article
- Non-Lynch Familial and Early-Onset Colorectal Cancer Explained by Accumulation of Low-Risk Genetic Variants.Cancers · 2021Article
- Colorectal cancer genetic variants are also associated with serrated polyposis syndrome susceptibility.Journal of medical genetics · 2020Article
- EIF3H promotes aggressiveness of esophageal squamous cell carcinoma by modulating Snail stability.Journal of experimental & clinical cancer research : CR · 2020Article
- Chromosomal Density of Cancer Up-Regulated Genes, Aberrant Enhancer Activity and Cancer Fitness Genes Are Associated with Transcriptional Cis-Effects of Broad Copy Number Gains in Colorectal Cancer.International journal of molecular sciences · 2019Article
- The role of 3D genome organization in disease: From compartments to single nucleotides.Seminars in cell & developmental biology · 2019Review
- Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer.Human genetics · 2019Article
- Positive Caricature Transcriptomic Effects Associated with Broad Genomic Aberrations in Colorectal Cancer.Scientific reports · 2018Article
- eIF3: a factor for human health and disease.RNA biology · 2018Review
- The non-coding variant rs1800734 enhances DCLK3 expression through long-range interaction and promotes colorectal cancer progression.Nature communications · 2017Article
- Hotspots of aberrant enhancer activity punctuate the colorectal cancer epigenome.Nature communications · 2017Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 4 countries.
Funding
Abstract
Common genetic variation at human 8q23.3 is significantly associated with colorectal cancer (CRC) risk. To elucidate the basis of this association we compared the frequency of common variants at 8q23.3 in 1,964 CRC cases and 2,081 healthy controls. Reporter gene studies showed that the single nucleotide polymorphism rs16888589 acts as an allele-specific transcriptional repressor. Chromosome conformation capture (3C) analysis demonstrated that the genomic region harboring rs16888589 interacts with the promoter of gene for eukaryotic translation initiation factor 3, subunit H (EIF3H). We show that increased expression of EIF3H gene increases CRC growth and invasiveness thereby providing a biological mechanism for the 8q23.3 association. These data provide evidence for a functional basis for the non-coding risk variant rs16888589 at 8q23.3 and provides novel insight into the etiological basis of CRC.
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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.