ArticleCancer science2008
Association between genetic polymorphisms of the base excision repair gene MUTYH and increased colorectal cancer risk in a Japanese population.
Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Meta-analysis of mismatch repair polymorphisms within the cogent consortium for colorectal cancer susceptibility.PloS one · 2013Pooled it
- Germline variants associated with breast cancer in Khakass women of North Asia.Molecular biology reports · 2023Article
- Association of base excision repair pathway genesInternational journal of occupational medicine and environmental health · 2022Article
- Clinical and genomic features of Chinese lung cancer patients with germline mutations.Nature communications · 2022Article
- Classification of the canonical splice alterationCold Spring Harbor molecular case studies · 2022Article
- DNA repair and cancer in colon and rectum: Novel players in genetic susceptibility.International journal of cancer · 2020Article
- Genetic Polymorphisms of DNA Repair Pathways in Sporadic Colorectal Carcinogenesis.Journal of Cancer · 2019Review
- 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
- Repair of 8-oxoG:A mismatches by the MUTYH glycosylase: Mechanism, metals and medicine.Free radical biology & medicine · 2017Review
- Lack of association between polymorphisms of the DNA base excision repair genes MUTYH and hOGG1 and keratoconus in a Polish subpopulation.Archives of medical science : AMS · 2015Article
- Article
- Increased risk for colorectal adenomas and cancer in mono-allelic MUTYH mutation carriers: results from a cohort of North-African Jews.Familial cancer · 2015Article
- A novel APC mosaicism in a patient with familial adenomatous polyposis.Human genome variation · 2015Article
- MUTYH-associated colorectal cancer and adenomatous polyposis.Surgery today · 2014Review
- Impaired 8-hydroxyguanine repair activity of MUTYH variant p.Arg109Trp found in a Japanese patient with early-onset colorectal cancer.Oxidative medicine and cellular longevity · 2014Article
- Cancer-associated variants and a common polymorphism of MUTYH exhibit reduced repair of oxidative DNA damage using a GFP-based assay in mammalian cells.Carcinogenesis · 2012Article
- Genetic variability in DNA repair proteins in age-related macular degeneration.International journal of molecular sciences · 2012Review
- MUTYH Tyr165Cys, OGG1 Ser326Cys and XPD Lys751Gln polymorphisms and head neck cancer susceptibility: a case control study.Molecular biology reports · 2011Article
- Identification of 5 novel germline APC mutations and characterization of clinical phenotypes in Japanese patients with classical and attenuated familial adenomatous polyposis.BMC research notes · 2010Article
- Adenine DNA glycosylase activity of 14 human MutY homolog (MUTYH) variant proteins found in patients with colorectal polyposis and cancer.Human mutation · 2010Article
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Authors and funding
17 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MUTYH gene encodes a DNA glycosylase that can initiate the base excision repair pathway and prevent G:C > T:A transversion by excising adenine mispaired with 8-hydroxyguanine. Biallelic germline mutations of MUTYH have been shown to predict familial and sporadic multiple colorectal adenomas and carcinomas, however, whether there is an association between single nucleotide polymorphisms (SNPs) of MUTYH and sporadic colorectal cancer (CRC) risk has remained unclear. In this study we investigated four MUTYH SNPs, IVS1+11C > T, IVS6+35G > A, IVS10-2A > G, and 972G > C (Gln324His), for an association with increased CRC risk in a population-based series of 685 CRC patients and 778 control subjects from Kyushu, Japan. A statistically significant association was demonstrated between IVS1+11T and increased CRC risk (odds ratio [OR]: 1.43; 95% confidence interval [CI]: 1.012-2.030; P = 0.042) and one of the five haplotypes based on the four SNPs, the IVS1+11T - IVS6+35G - IVS10-2A - 972C (TGAC) haplotype containing IVS1+11T, was demonstrated to be associated with increased CRC risk (OR, 1.43; 95% CI, 1.005-2.029; P = 0.046). Subsite-specific analysis showed that the TGAC haplotype was statistically significantly (P = 0.013) associated with an increased risk of distal colon, but not proximal colon or rectal cancer. Furthermore, IVS1+11C > T was found to be in complete linkage disequilibrium with -280G > A and 1389G > C (Thr463Thr). The results indicated that Japanese individuals with - 280A/IVS1+11T/1389C genotypes or the TGAC haplotype are susceptible to CRC.
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