ReviewOncogene2022
MUTYH-associated tumor syndrome: The other face of MAP.
Review in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 31 citations in OpenAlex.
- DNA Damage Recognition by Bacterial and Human Adenine-DNA Glycosylases: Insights from Non-Canonical Substrates.Biomolecules · 2026Article
- TruncatingJournal of cancer prevention · 2026Article
- Regulatory networks of iron sulfur cluster biology in cancer mechanisms and therapeutic perspectives.iScience · 2026Review
- KRAS-G12C: The neglected biomarker to detect patients with MUTYH-associated polyposis.International journal of cancer · 2026Article
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- An intriguing journey into the hereditary syndromes predisposing to endometrial cancer: more than believed.Therapeutic advances in medical oncology · 2026Review
- Clinical Utility of Whole-Genome Sequencing to Aid Histologic Diagnosis and to Direct Personalized Medicine in Salivary Gland Cancer.JCO precision oncology · 2025Article
- Prevalence of MUTYH Monoallelic Variants in Patients With Hereditary Cancer Using Multigene Panel Testing.Cancer medicine · 2025Article
- Review
- Structure of human MUTYH and functional profiling of cancer-associated variants reveal an allosteric network between its [4Fe-4S] cluster cofactor and active site required for DNA repair.Nature communications · 2025Article
- Hereditary Colorectal Cancer: Clinical Implications of Genomic Medicine and Precision Oncology.Journal of the anus, rectum and colon · 2025Review
- A brief review of Lynch syndrome: understanding the dual cancer risk between endometrial and colorectal cancer.Oncology reviews · 2025Review
- A Novel GermlineHuman mutation · 2025Article
- A comprehensive characterization of the spectrum of MUTYH germline pathogenic variants in Latin America.Familial cancer · 2024Article
- Hereditary Gastrointestinal Tumor Syndromes: When Risk Comes with Your Genes.Current issues in molecular biology · 2024Review
- Identification of Genes with Rare Loss of Function Variants Associated with Aggressive Prostate Cancer and Survival.European urology oncology · 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
- Phenotype Correlations With Pathogenic DNA Variants in theHuman mutation · 2024Review
- Screening for Mutations in Hereditary Cancer Susceptibility Genes in a Region with High Endogamy in Brazil.Global medical genetics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MUTYH gene is involved in the base excision repair (BER) mechanism and its pathogenic alterations are associated with colorectal polyposis and cancer. MUTYH-associated polyposis (MAP) is a condition which is inherited in an autosomal recessive manner. MAP patients, beyond colorectal cancer (CRC), may develop other types of tumors, including duodenal, breast, ovarian, pancreatic, bladder and skin cancers. Carriers of biallelic MUTYH likely pathogenic/pathogenic variants exhibit a high lifetime risk of CRC, though cancer risk evidence becomes less clear when monoallelic carriers and extraintestinal tumors are considered. However, several studies recently reported an increased genetic susceptibility to cancer also for carriers of germline monoallelic MUTYH mutations. Moreover, experimental evidence highlighted the MUTYH involvement in many other biological functions. In future, MUTYH mutation carriers might benefit from new target therapies involving the use of PD-1 or KRAS inhibitors. Therefore, "MUTYH-associated tumor syndrome" might be the most appropriate term, due to the multiplicity of tumors observed in MAP patients and different biological contexts in which MUTYH acts as a "playmaker". In this Review, we will investigate the impact of germline mono- and biallelic MUTYH mutations on cancer risk, providing a proposal for clinical surveillance of mutation carriers.
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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.