ReviewGut2015
Genetic architecture of colorectal cancer.
Review in Gut, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 3 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
110 citing papers in PubMed, 3 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- Genome-Wide Association Analyses of Equine Metabolic Syndrome Phenotypes in Welsh Ponies and Morgan Horses.Genes · 2019Pooled it
- Large-Scale Genome-Wide Association Study of East Asians Identifies Loci Associated With Risk for Colorectal Cancer.Gastroenterology · 2019Pooled it
- Diagnostic and prognostic value of miR-106a in colorectal cancer.Oncotarget · 2017Pooled it
- The association between EGF A61G polymorphism and risk of colorectal cancer in a Chinese population: a case-control study.Bioscience reports · 2019Trial
- MyGeneRisk Colon: A Web-Based Tool for Personalized Colorectal Cancer Risk Prediction Based on Genetics and Lifestyle.medRxiv : the preprint server for health sciences · 2026Article
- Genetic landscape of Chinese colorectal cancer: insights into germline and somatic mutations.BMC cancer · 2026Article
- A Multiomic Approach Integrating Genomic and Metabolomic Data Highlights Colorectal Cancer Pathways.Journal of proteome research · 2026Article
- Multiple polygenic score approach in colorectal cancer risk prediction.Scientific reports · 2025Article
- Exploring the Role ofJournal of clinical medicine · 2025Article
- Investigating the role of the Pon1-rs854560 (L55M) SNP in colorectal Cancer susceptibility.Journal of cancer research and clinical oncology · 2025Article
- GAS5 rs145204276 Ins/Del Polymorphism Is Associated with CRC Susceptibility in a Romanian Population.International journal of molecular sciences · 2025Article
- Study of Microbiota Associated to Early Tumors Can Shed Light on Colon Carcinogenesis.International journal of molecular sciences · 2024Review
- Urocortin-1 promotes colorectal cancer cell migration and proliferation and inhibits apoptosis via inhibition of the p53 signaling pathway.Journal of cancer research and clinical oncology · 2024Article
- Assessments of dietary intake and polygenic risk score in associations with colorectal cancer risk: evidence from the UK Biobank.BMC cancer · 2023Article
- Prevalence and genetic spectrum associated with hereditary colorectal cancer syndromes, the need to improve cancer risk awareness, and family cascade testing in Vietnam.Familial cancer · 2023Article
- A Genetic Locus within the FMN1/GREM1 Gene Region Interacts with Body Mass Index in Colorectal Cancer Risk.Cancer research · 2023Article
- Review
- The Largest Chinese Cohort Study Indicates Homologous Recombination Pathway Gene Mutations as Another Major Genetic Risk Factor for Colorectal Cancer with Heterogeneous Clinical Phenotypes.Research (Washington, D.C.) · 2023Article
- PITX1 plays essential functions in cancer.Frontiers in oncology · 2023Review
- Changing Colorectal Cancer Trends in Asians: Epidemiology and Risk Factors.Oncology reviews · 2023Review
50 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is a complex disease that develops as a consequence of both genetic and environmental risk factors. A small proportion (3-5%) of cases arise from hereditary syndromes predisposing to early onset CRC as a result of mutations in over a dozen well defined genes. In contrast, CRC is predominantly a late onset 'sporadic' disease, developing in individuals with no obvious hereditary syndrome. In recent years, genome wide association studies have discovered that over 40 genetic regions are associated with weak effects on sporadic CRC, and it has been estimated that increasingly large genome wide scans will identify many additional novel genetic regions. Subsequent experimental validations have identified the causally related variant(s) in a limited number of these genetic regions. Further biological insight could be obtained through ethnically diverse study populations, larger genetic sequencing studies and development of higher throughput functional experiments. Along with inherited variation, integration of the tumour genome may shed light on the carcinogenic processes in CRC. In addition to summarising the genetic architecture of CRC, this review discusses genetic factors that modify environmental predictors of CRC, as well as examples of how genetic insight has improved clinical surveillance, prevention and treatment strategies. In summary, substantial progress has been made in uncovering the genetic architecture of CRC, and continued research efforts are expected to identify additional genetic risk factors that further our biological understanding of this disease. Subsequently these new insights will lead to improved treatment and prevention of colorectal cancer.
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.