ArticleThe Journal of pathology2016
Adenoma development in familial adenomatous polyposis and MUTYH-associated polyposis: somatic landscape and driver genes.
Article in The Journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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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.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Unveiling the protein landscape for early detection of colorectal precancerous lesions.Clinical proteomics · 2025Article
- Colorectal carcinogenesis in the Lynch syndromes and familial adenomatous polyposis: trigger events and downstream consequences.Hereditary cancer in clinical practice · 2025Review
- Article
- PIGA Mutations and Glycosylphosphatidylinositol Anchor Dysregulation in Polyposis-Associated Duodenal Tumorigenesis.Molecular cancer research : MCR · 2024Article
- Cellular Repair of Synthetic Analogs of Oxidative DNA Damage Reveals a Key Structure-Activity Relationship of the Cancer-Associated MUTYH DNA Repair Glycosylase.ACS central science · 2024Article
- Oxidative stress accelerates intestinal tumorigenesis by enhancing 8-oxoguanine-mediated mutagenesis in MUTYH-deficient mice.Genome research · 2024Article
- Increased KRAS G12C Prevalence, High Tumor Mutational Burden, and Specific Mutational Signatures Are Associated With MUTYH Mutations: A Pan-Cancer Analysis.The oncologist · 2024Article
- Evolutionary history of adenomas to colorectal cancer in FAP families.Frontiers in genetics · 2024Article
- Inherited MUTYH mutations cause elevated somatic mutation rates and distinctive mutational signatures in normal human cells.Nature communications · 2022Article
- Mathematical modeling of multiple pathways in colorectal carcinogenesis using dynamical systems with Kronecker structure.PLoS computational biology · 2021Article
- Discovering the Mutational Profile of Early Colorectal Lesions: A Translational Impact.Cancers · 2021Review
- Article
- Review
- Variant profiling of colorectal adenomas from three patients of two families with MSH3-related adenomatous polyposis.PloS one · 2021Article
- Impact ofMicroorganisms · 2020Article
- Article
- The genomics of oxidative DNA damage, repair, and resulting mutagenesis.Computational and structural biotechnology journal · 2020Review
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- AACR White Paper: Shaping the Future of Cancer Prevention - A Roadmap for Advancing Science and Public Health.Cancer prevention research (Philadelphia, Pa.) · 2018Article
- Mutational signature distribution varies with DNA replication timing and strand asymmetry.Genome biology · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP) are inherited disorders associated with multiple colorectal adenomas that lead to a very high risk of colorectal cancer. The somatic mutations that drive adenoma development in these conditions have not been investigated comprehensively. In this study we performed analysis of paired colorectal adenoma and normal tissue DNA from individuals with FAP or MAP, sequencing 14 adenoma whole exomes (eight MAP, six FAP), 55 adenoma targeted exomes (33 MAP, 22 FAP) and germline DNA from each patient, and a further 63 adenomas by capillary sequencing (41 FAP, 22 MAP). With these data we examined the profile of mutated genes, the mutational signatures and the somatic mutation rates, observing significant diversity in the constellations of mutated driver genes in different adenomas, and loss-of-function mutations in WTX (9%; p < 9.99e-06), a gene implicated in regulation of the WNT pathway and p53 acetylation. These data extend our understanding of the early events in colorectal tumourigenesis in the polyposis syndromes.
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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.