ArticleCarcinogenesis2014
Identification of candidate susceptibility genes for colorectal cancer through eQTL analysis.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 3 of them syntheses that pooled it.
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Who cites it
49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 91 citations in OpenAlex.
- Alcohol consumption, DNA methylation and colorectal cancer risk: Results from pooled cohort studies and Mendelian randomization analysis.International journal of cancer · 2022Pooled it
- A comprehensive meta-analysis of genetic associations between five key SNPs and colorectal cancer risk.Oncotarget · 2016Pooled it
- Pooled it
- DIP2B as a Prognostic Biomarker and Immunotherapy Target: Insights from Pan-Cancer Analysis.Applied biochemistry and biotechnology · 2026Article
- Integrative eQTL and Mendelian randomization analysis reveals key genes in colorectal cancer.Discover oncology · 2025Article
- Targeting colorectal cancer at the level of nuclear pore complex.Journal of advanced research · 2025Review
- Comprehensive identification of hub mRNAs and lncRNAs in colorectal cancer using galaxy: an in silico transcriptome analysis.Discover oncology · 2025Article
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- Single-cell transcriptomics reveals long noncoding RNAs associated with tumor biology and the microenvironment in pancreatic cancer.NAR cancer · 2023Article
- Integrated pancancer analysis reveals the oncogene characteristics and prognostic value of DIP2B in breast cancer.BMC cancer · 2023Article
- HSP90AA1 promotes lymphatic metastasis of hypopharyngeal squamous cell carcinoma by regulating epithelial-mesenchymal transition.Oncology research · 2023Article
- A novel DNA methylation-driver gene signature for long-term survival prediction of hepatitis-positive hepatocellular carcinoma patients.Cancer medicine · 2022Article
- Endoplasmic reticulum-resident protein Sec62 drives colorectal cancer metastasis via MAPK/ATF2/UCA1 axis.Cell proliferation · 2022Article
- Transcriptional dynamics of colorectal cancer risk associated variation at 11q23.1 correlate with tuft cell abundance and marker expression in silico.Scientific reports · 2022Article
- Bisphenol A replacement chemicals, BPF and BPS, induce protumorigenic changes in human mammary gland organoid morphology and proteome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Many Faces of G Protein-Coupled Receptor 143, an Atypical Intracellular Receptor.Frontiers in molecular biosciences · 2022Review
- Repurposing non-invasive prenatal testing data: Population study of single nucleotide variants associated with colorectal cancer and Lynch syndrome.Oncology letters · 2021Article
- AHA1 regulates cell migration and invasion via the EMT pathway in colorectal adenocarcinomas.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
In this study, we aim to identify the genes responsible for colorectal cancer risk behind the loci identified in genome-wide association studies (GWAS). These genes may be candidate targets for developing new strategies for prevention or therapy. We analyzed the association of genotypes for 26 GWAS single nucleotide polymorphisms (SNPs) with the expression of genes within a 2 Mb region (cis-eQTLs). Affymetrix Human Genome U219 expression arrays were used to assess gene expression in two series of samples, one of healthy colonic mucosa (n = 47) and other of normal mucosa adjacent to colon cancer (n = 97, total 144). Paired tumor tissues (n = 97) were also analyzed but did not provide additional findings. Partial Pearson correlation (r), adjusted for sample type, was used for the analysis. We have found Bonferroni-significant cis-eQTLs in three loci: rs3802842 in 11q23.1 associated to C11orf53, COLCA1 (C11orf92) and COLCA2 (C11orf93; r = 0.60); rs7136702 in 12q13.12 associated to DIP2B (r = 0.63) and rs5934683 in Xp22.3 associated to SHROOM2 and GPR143 (r = 0.47). For loci in chromosomes 11 and 12, we have found other SNPs in linkage disequilibrium that are more strongly associated with the expression of the identified genes and are better functional candidates: rs7130173 for 11q23.1 (r = 0.66) and rs61927768 for 12q13.12 (r = 0.86). These SNPs are located in DNA regions that may harbor enhancers or transcription factor binding sites. The analysis of trans-eQTLs has identified additional genes in these loci that may have common regulatory mechanisms as shown by the analysis of protein-protein interaction networks.
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