ArticleMutagenesis2012
Investigation of the effects of DNA repair gene polymorphisms on the risk of colorectal cancer.
Article in Mutagenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 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
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Association between XRCC1 and XRCC3 polymorphisms and colorectal cancer risk: a meta-analysis of 23 case-control studies.Molecular biology reports · 2013Pooled it
- Pooled it
- XRCC2 gene polymorphisms and its protein are associated with colorectal cancer susceptibility in Chinese Han population.Medical oncology (Northwood, London, England) · 2014Trial
- Targeted Sequencing of Plasma-Derived vs. Urinary cfDNA from Patients with Triple-Negative Breast Cancer.Cancers · 2022Article
- MLH1 single-nucleotide variant in circulating tumor DNA predicts overall survival of patients with hepatocellular carcinoma.Scientific reports · 2020Article
- DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers.International journal of molecular sciences · 2020Review
- DNA repair and cancer in colon and rectum: Novel players in genetic susceptibility.International journal of cancer · 2020Article
- Single nucleotide polymorphisms inOncotarget · 2017Article
- The Association of Low-Penetrance Variants in DNA Repair Genes with Colorectal Cancer: A Systematic Review and Meta-Analysis.Clinical and translational gastroenterology · 2017Article
- Gut Microbiota Imbalance and Base Excision Repair Dynamics in Colon Cancer.Journal of Cancer · 2016Review
- APE1 polymorphisms are associated with colorectal cancer susceptibility in Chinese Hans.World journal of gastroenterology · 2014Article
- Nucleotide excision repair gene polymorphisms, meat intake and colon cancer risk.Mutation research · 2014Article
- New insights and clinical advancements in cellular oncology.Cellular oncology (Dordrecht, Netherlands) · 2012Article
- Colorectal cancer: A review of the genome-wide association studies in the kingdom of Saudi Arabia.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Despite their prime candidate status, polymorphisms near genes involved in DNA repair or in other functions related to genome stability have been conspicuously under-represented in the significant associations reported from genome-wide association studies (GWAS) of cancer susceptibility. In this study, we assessed a set of single-nucleotide polymorphisms (SNPs) near 157 DNA repair genes in three colorectal cancer (CRC) GWAS. Although no individual SNP showed evidence of association, the set of SNPs as a whole was associated with colorectal cancer risk. When candidate SNPs were examined, our data did not support most of the previously reported associations with CRC susceptibility, an exception being an effect of the MLH1 promoter SNP -93G>A (rs1800734). Rare variants in CHEK2 (I157T and possibly del1100C) also appear to be associated with CRC risk. Overall, the absence to date of disease-associated DNA repair SNPs in cancer GWAS may be explained by a combination of the following: (i) many loci with individually very small effects on risk; (ii) rare alleles of moderate effect and (iii) subgroups of CRC, such as those with microsatellite instability, associated with specific variants. It will be particularly intriguing to determine whether any GWAS across cancer types identify DNA variants that predispose to cancers of more than one site.
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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.