SynthesisPloS one2013
Meta-analysis of mismatch repair polymorphisms within the cogent consortium for colorectal cancer susceptibility.
Synthesis in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis 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, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Association between MutL homolog 1 polymorphisms and the risk of colorectal cancer: a meta-analysis.Journal of cancer research and clinical oncology · 2015Pooled it
- The MLH1 c.1852_1853delinsGC (p.K618A) variant in colorectal cancer: genetic association study in 18,723 individuals.PloS one · 2014Trial
- Polymorphisms in Base Excision Repair Genes and Association with Multiple Sclerosis in a Pilot Study on a Central European Population.International journal of molecular sciences · 2025Article
- MUTYH-associated tumor syndrome: The other face of MAP.Oncogene · 2022Review
- DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers.International journal of molecular sciences · 2020Review
- Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases in Colorectal Cancer Patients.International journal of molecular sciences · 2020Review
- Results of multigene panel testing in familial cancer cases without genetic cause demonstrated by single gene testing.Scientific reports · 2019Article
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- From colorectal cancer pattern to the characterization of individuals at risk: Picture for genetic research in Latin America.International journal of cancer · 2019Review
- Identification of genetic variants for clinical management of familial colorectal tumors.BMC medical genetics · 2018Article
- The Association of Low-Penetrance Variants in DNA Repair Genes with Colorectal Cancer: A Systematic Review and Meta-Analysis.Clinical and translational gastroenterology · 2017Article
- DNA repair genes polymorphisms and genetic susceptibility to Philadelphia-negative myeloproliferative neoplasms in a Portuguese population: The role of base excision repair genes polymorphisms.Oncology letters · 2017Article
- Association of monoallelic MUTYH mutation among Egyptian patients with colorectal cancer.Familial cancer · 2017Article
- MLH1 Ile219Val Polymorphism in Argentinean Families with Suspected Lynch Syndrome.Frontiers in oncology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
37 authors at 19 institutions in 10 countries.
Funding
Abstract
In the last four years, Genome-Wide Association Studies (GWAS) have identified sixteen low-penetrance polymorphisms on fourteen different loci associated with colorectal cancer (CRC). Due to the low risks conferred by known common variants, most of the 35% broad-sense heritability estimated by twin studies remains unexplained. Recently our group performed a case-control study for eight Single Nucleotide Polymorphisms (SNPs) in 4 CRC genes. The present investigation is a follow-up of that study. We have genotyped six SNPs that showed a positive association and carried out a meta-analysis based on eight additional studies comprising in total more than 8000 cases and 6000 controls. The estimated recessive odds ratio for one of the SNPs, rs3219489 (MUTYH Q338H), decreased from 1.52 in the original Swedish study, to 1.18 in the Swedish replication, and to 1.08 in the initial meta-analysis. Since the corresponding summary probability value was 0.06, we decided to retrieve additional information for this polymorphism. The incorporation of six further studies resulted in around 13000 cases and 13000 controls. The newly updated OR was 1.03. The results from the present large, multicenter study illustrate the possibility of decreasing effect sizes with increasing samples sizes. Phenotypic heterogeneity, differential environmental exposures, and population specific linkage disequilibrium patterns may explain the observed difference of genetic effects between Sweden and the other investigated cohorts.
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.