ArticleFamilial cancer2012
Common MUTYH mutations and colorectal cancer risk in multiethnic populations.
Article in Familial cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Characterizing germline APC and MUTYH variants in Ashkenazi Jews compared to other individuals.Familial cancer · 2021Article
- Hormonal and reproductive factors and reduction in the risk of colorectal cancer.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2020Observational
- Association of a New Germline Variant in the MUTYH DNA Glycosylase Gene with Colorectal Adenoma Transformation into MalignancyIranian biomedical journal · 2019Article
- Base excision repair deficiency signatures implicate germline and somaticCold Spring Harbor molecular case studies · 2019Article
- Incidental and clinically actionable genetic variants in 1005 whole exomes and genomes from Qatar.Molecular genetics and genomics : MGG · 2018Article
- Increased risk for colorectal adenomas and cancer in mono-allelic MUTYH mutation carriers: results from a cohort of North-African Jews.Familial cancer · 2015Article
- MUTYH-associated polyposis (MAP): evidence for the origin of the common European mutations p.Tyr179Cys and p.Gly396Asp by founder events.European journal of human genetics : EJHG · 2014Article
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
MUTYH is associated with colorectal cancer (CRC) risk. We studied the frequency of MUTYH and risk of CRC in Arabs, North African and European Jews. Participants were all 593 Sephardi Moroccan Jews (232 cases, 361 controls) and all 631 Arabs (327 cases, 304 controls) recruited into a population-based study of colorectal cancer in Israel, as well as a random sample of 189 Ashkenazi Jewish cases. Two MUTYH mutations, G396D and Y179C, were studied in 1,413 individuals, with MUTYH sequence analysis in 46 cases with CRC in a sibling or adenoma. No carriers of mutations in MUTYH were identified in Ashkenazi Jews and only one in Arabs. In Sephardi Jews, 28 carriers of G396D, 25 (4.2%) heterozygotes and 3 (0.5%) homozygotes were identified. Four (0.7%) were heterozygote carriers of the Y179C mutation. Two compound heterozygous carriers of Y179C and G396D were identified. Homozygote carriers of G396D had nonsignificantly elevated risk of CRC (OR = 11.0, 95% CI: 0.91-213.9, p = 0.06), and combined bi-allelic carriers of G396D and Y179C had increased risk, OR = 17.4, 95% CI = (1.9-316.7, p = 0.009). Four of five bi-allelic carriers reported a family history of CRC. Sequencing of 46 colorectal cancer cases with family history and additional adenomas, did not identify any other non-founder mutations. MUTYH carriers of the two common founder mutations are profoundly under-represented among both Ashkenazi Jews and Arabs. The prevalence of MUTYH carriers of the common mutations is much higher in Sephardi Jews. Bi-allelic carriers of mutations in MUTYH, are associated with highly risk of colorectal cancer.
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