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 common cancer-associated DNA polymerase ε mutation causes an exceptionally strong mutator phenotype, indicating fidelity defects distinct from loss of proofreading.

Cancer research - 1 Apr 2014

Kane Daniel P, Shcherbakova Polina V

Abstract excerpt

Exonucleolytic proofreading and DNA mismatch repair (MMR) act in series to maintain high-fidelity DNA replication and to avoid mutagenesis. MMR defects elevate the overall mutation rate and are associated with increased cancer incidence. Hypermutable colorectal and endometrial tumors with functional MMR were recently reported to carry amino acid substitutions in the exonuclease domain of DNA polymerase ε (Polε)....

Read the complete abstract on PubMed

Topics

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

Share to Amino Acid Sequence
Share to Cancer Genomics and Diagnostics

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Colorectal Neoplasms

Share to DNA Polymerase II

Share to Genetic factors in colorectal cancer

Share to Molecular Sequence Data

Share to Mutation

Share to Phenotype

Source

Open in PubMed Open full text

Identifiers

PMID: 24525744
DOI: 10.1158/0008-5472.CAN-13-2892
PMCID: PMC4310866

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A common cancer-associated DNA polymerase ε mutation causes an exceptionally strong mutator phenotype, indicating fidelity defects distinct from loss of proofreading.PMID 24525744Read ↗

Functional Analysis of Cancer-Associated DNA Polymerase ε Variants in Saccharomyces cerevisiae.Semantic proximity Read ↗

Explosive mutation accumulation triggered by heterozygous human Pol ε proofreading-deficiency is driven by suppression of mismatch repairSemantic proximity Read ↗

Mutagenic mechanisms of cancer-associated DNA polymerase ε allelesSemantic proximity Read ↗

A panoply of errors: polymerase proofreading domain mutations in cancer.Semantic proximity Read ↗

Replicative DNA polymerase defects in human cancers: Consequences, mechanisms, and implications for therapy.Semantic proximity Read ↗

Comparative Analysis of Somatic and Germline Polymerase Proofreading Deficiencies in Cancer: Molecular and Clinical Implications.Semantic proximity Read ↗

Mutagenic mechanisms of cancer-associated DNA polymerase ϵ alleles.Semantic proximity Read ↗

Enhanced polymerase activity permits efficient synthesis by cancer-associated DNA polymerase ϵ variants at low dNTP levels.Semantic proximity Read ↗

Human Pol ε-dependent replication errors and the influence of mismatch repair on their correction.Semantic proximity Read ↗

DNA Polymerase ɛ Deficiency Leading to an Ultramutator Phenotype: A Novel Clinically Relevant Entity.Semantic proximity Read ↗

POLE Mutation Spectra Are Shaped by the Mutant Allele Identity, Its Abundance, and Mismatch Repair Status.Semantic proximity Read ↗

DNA polymerase ε and δ variants drive mutagenesis in polypurine tracts in human tumors.Semantic proximity Read ↗

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