ArticleGut2025
Genetic variation at 11q23.1 confers colorectal cancer risk by dysregulation of colonic tuft cell transcriptional activator
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Therapeutic implications of targeting cancer testis antigen MAGEA1 in cervical cancer.International journal of oncology · 2026Article
- Key genes and pathway differences between serrated polyps and conventional adenomas: insights from multi-omics.Translational cancer research · 2026Article
- A conserved 3'UTR short motif regulates gene expression in vertebrates.Nucleic acids research · 2026Article
- Review
- Multi-tissue expression and splicing data prioritise anatomical subsite- and sex-specific colorectal cancer susceptibility genes.Nature communications · 2025Article
- Systematic prioritization of functional variants and effector genes underlying colorectal cancer risk.Nature genetics · 2024Article
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
backgroundCommon genetic variation at 11q23.1 is associated with colorectal cancer (CRC) risk, exerting local expression quantitative trait locus (cis-eQTL) effects on
objectiveUndertake an interdisciplinary approach to understand how variation at 11q23.1 locus imparts CRC risk.
designWe employ analysis of RNA sequencing, single-cell RNA sequencing, chromatin immunoprecipitation sequencing and single-cell ATAC sequencing data to identify, prioritise and characterise the genes that contribute to CRC risk. We further validate these findings using mouse models and demonstrate parallel effects in human colonic mucosa.
resultsWe establish rs3087967 as a prime eQTL variant at 11q23.1, colocalising with CRC risk. Furthermore, rs3087967 influences expression of 21 distant genes, thereby acting as a trans-eQTL hub for a gene-set highly enriched for tuft cell markers. Epigenomic analysis implicates POU2AF2 as controlling the tuft cell-specific trans-genes, through POU2F3-correlated genomic regulation. Immunofluorescence confirms rs3087967 risk genotype (T) to be associated with a tuft cell deficit in the human colon. CRISPR-mediated deletion of the 11q23.1 risk locus genes in the mouse germline exacerbated the
conclusionWe demonstrate that genotype at rs3087967 controls a portfolio of genes through misregulation of
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