Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A Specific Mutational Signature Associated with DNA 8-Oxoguanine Persistence in MUTYH-defective Colorectal Cancer.

EBioMedicine - 1 Jun 2017

Viel Alessandra, Bruselles Alessandro, Meccia Ettore, Fornasarig Mara, Quaia Michele, Canzonieri Vincenzo, Policicchio Eleonora, Urso Emanuele Damiano, Agostini Marco, Genuardi Maurizio, Lucci-Cordisco Emanuela, Venesio Tiziana, Martayan Aline, Diodoro Maria Grazia, Sanchez-Mete Lupe, Stigliano Vittoria, Mazzei Filomena, Grasso Francesca, Giuliani Alessandro, Baiocchi Marta, Maestro Roberta, Giannini Giuseppe, Tartaglia Marco, Alexandrov Ludmil B, Bignami Margherita

Abstract excerpt

8-Oxoguanine, a common mutagenic DNA lesion, generates G:C>T:A transversions via mispairing with adenine during DNA replication. When operating normally, the MUTYH DNA glycosylase prevents 8-oxoguanine-related mutagenesis by excising the incorporated adenine. Biallelic MUTYH mutations impair this enzymatic function and are associated with colorectal cancer (CRC) in MUTYH-Associated Polyposis (MAP) syndrome. Here,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA Damage

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA Glycosylases

Share to Exome Sequencing

Share to Genes, Tumor Suppressor

Share to Guanine

Share to Microsatellite Instability

Share to Mutation Rate

Share to Oncogenes

Source

Open in PubMed Open full text

Identifiers

PMID: 28551381
DOI: 10.1016/j.ebiom.2017.04.022
PMCID: PMC5478212

Genes

MUTYH
AMER1
APC
FAT1
FAT4
KRAS
SMAD2
SMAD4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Specific Mutational Signature Associated with DNA 8-Oxoguanine Persistence in MUTYH-defective Colorectal Cancer.PMID 28551381Read ↗

Germline haploinsufficiency for the base excision repair gene <i>MUTYH</i> causes mutational signature SBS18 in multiple tumour types, specifically leading to an increased risk of colorectal cancerSemantic proximity Read ↗

Inherited MUTYH mutations cause elevated somatic mutation rates and distinctive mutational signatures in normal human cells.Semantic proximity Read ↗

Mutational signature analysis identifies MUTYH deficiency in colorectal cancers and adrenocortical carcinomas.Semantic proximity Read ↗

MUTYH-associated polyposis--from defect in base excision repair to clinical genetic testing.Semantic proximity Read ↗

Unraveling the genomic landscape of colorectal cancer through mutational signatures.Semantic proximity Read ↗

Evaluating the utility of tumour mutational signatures for identifying hereditary colorectal cancer and polyposis syndrome carriersSemantic proximity Read ↗

Role of MUTYH in human cancer.Semantic proximity Read ↗

Endometrial cancer may be part of the MUTYH-associated polyposis cancer spectrum.Semantic proximity Read ↗

Oxidative stress accelerates intestinal tumorigenesis by enhancing 8-oxoguanine-mediated mutagenesis in MUTYH-deficient mice.Semantic proximity Read ↗

Evaluating the utility of tumour mutational signatures for identifying hereditary colorectal cancer and polyposis syndrome carriers.Semantic proximity Read ↗

Incident Cancer Risk and Signatures Among Older MUTYH Carriers: Analysis of Population-Based and Genomic Cohorts.Semantic proximity Read ↗

First report of medulloblastoma in a patient with MUTYH-associated polyposis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.