ArticleNature communications2014
Functional annotation of colon cancer risk SNPs.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 4 of them syntheses that pooled 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.
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
78 citing papers in PubMed, 4 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- Genome-wide association studies and Mendelian randomization analyses provide insights into the causes of early-onset colorectal cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2024Pooled it
- Integrated meta-analysis of colorectal cancer public proteomic datasets for biomarker discovery and validation.PLoS computational biology · 2024Pooled it
- Genetic polymorphisms of CYP24A1 gene and cancer susceptibility: a meta-analysis including 40640 subjects.World journal of surgical oncology · 2023Pooled it
- Association between the HOTAIR polymorphisms and cancer risk: an updated meta-analysis.Oncotarget · 2017Pooled it
- Mixed-model and transcriptome-wide association analyses identify transcription factors and genes associated with colorectal cancer susceptibility.Nature communications · 2026Article
- A review of post-GWAS studies in schizophrenia.Translational psychiatry · 2025Review
- Single-cell multi-omics analysis reveals cancer regulatory elements of transcriptional programs and clinical implications.Cell death & disease · 2025Article
- The Genomic Topography of Appendiceal Cancers: Our Current Understanding, Clinical Perspectives, and Future Directions.Cancers · 2025Review
- Article
- Functional dissection of noncoding variants associated with rheumatoid arthritis.Annals of the rheumatic diseases · 2025Article
- The genetic landscape of CYP24A1 polymorphisms in cancer risk: evidence from a systematic review.Discover oncology · 2025Review
- Association of MiRNA Polymorphisms Involved in the PI3K/ATK/GSK3β Pathway with T2DM in a Chinese Population.Pharmacogenomics and personalized medicine · 2025Article
- Identification of Novel lncRNAs Related to Colorectal Cancer Through Bioinformatics Analysis.BioMed research international · 2025Article
- An oncogenic enhancer promotes melanoma progression via regulating ETV4 expression.Journal of translational medicine · 2024Article
- The Clinical Significance of MicroRNAs in Colorectal Cancer Signaling Pathways: A Review.Global medical genetics · 2023Review
- Emerging insights into enhancer biology and function.Transcription · 2023Review
- Exome-based new allele-specific PCR markers and transferability for sodicity tolerance in bread wheat (Plant direct · 2023Article
- Article
- Application of CRISPR-Cas9 gene editing technology in basic research, diagnosis and treatment of colon cancer.Frontiers in endocrinology · 2023Review
- Role of Non-Coding RNAs in Colorectal Cancer: Focus on Long Non-Coding RNAs.International journal of molecular sciences · 2022Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is a leading cause of cancer-related deaths in the United States. Genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with increased risk for CRC. A molecular understanding of the functional consequences of this genetic variation has been complicated because each GWAS SNP is a surrogate for hundreds of other SNPs, most of which are located in non-coding regions. Here we use genomic and epigenomic information to test the hypothesis that the GWAS SNPs and/or correlated SNPs are in elements that regulate gene expression, and identify 23 promoters and 28 enhancers. Using gene expression data from normal and tumour cells, we identify 66 putative target genes of the risk-associated enhancers (10 of which were also identified by promoter SNPs). Employing CRISPR nucleases, we delete one risk-associated enhancer and identify genes showing altered expression. We suggest that similar studies be performed to characterize all CRC risk-associated enhancers.
Indexed as
Identifiers
What OpenQuestion holds
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.