Associated Papers
Phenotypic POLE Variant Classification Identifies Patients Who May Have Favorable Prognosis and Benefit from Immunotherapy.
Keller-Evans RB et al.
The Journal of Molecular Diagnostics : Jmd, 2026
The proofreading mechanism of the human leading-strand DNA polymerase ε holoenzyme.
Wang F et al.
Proceedings of the National Academy of Sciences of the United States of America, 2025
The proofreading mechanism of the human leading strand DNA polymerase ε holoenzyme.
Wang F et al.
Biorxiv : the Preprint Server for Biology, 2025
Structural basis for processive daughter-strand synthesis and proofreading by the human leading-strand DNA polymerase Pol ε.
Roske JJ et al.
Nature Structural & Molecular Biology, 2024
Human DNA polymerase ε is a source of C>T mutations at CpG dinucleotides.
Tomkova M et al.
Nature Genetics, 2024
Structures of the human leading strand Polε-PCNA holoenzyme.
He Q et al.
Nature Communications, 2024
Deep learning for dual detection of microsatellite instability and POLE mutations in colorectal cancer histopathology.
Gustav M et al.
Npj Precision Oncology, 2024
Exploring the basis of heterogeneity of cancer aggressiveness among the mutated POLE variants.
Selves J et al.
Life Science Alliance, 2024
A simple bypass assay for DNA polymerases shows that cancer-associated hypermutating variants exhibit differences in vitro.
Crevel G et al.
The Febs Journal, 2023
Recommendations for the classification of germline variants in the exonuclease domain of POLE and POLD1.
Mur P et al.
Genome Medicine, 2023
CTF18-RFC contributes to cellular tolerance against chain-terminating nucleoside analogs (CTNAs) in cooperation with proofreading exonuclease activity of DNA polymerase ε.
Washif M et al.
Dna Repair, 2023
The hereditary N363K POLE exonuclease mutant extends PPAP tumor spectrum to glioblastomas by causing DNA damage and aneuploidy in addition to increased mismatch mutagenicity.
Labrousse G et al.
Nar Cancer, 2023
Characterization of POLE c.1373A > T p.(Tyr458Phe), causing high cancer risk.
Rocque MJ et al.
Molecular Genetics and Genomics : Mgg, 2023
Probing the mechanisms of two exonuclease domain mutators of DNA polymerase ϵ.
Dahl JM et al.
Nucleic Acids Research, 2022
Cancers from Novel Pole-Mutant Mouse Models Provide Insights into Polymerase-Mediated Hypermutagenesis and Immune Checkpoint Blockade.
Galati MA et al.
Cancer Research, 2020
POLE Mutation Spectra Are Shaped by the Mutant Allele Identity, Its Abundance, and Mismatch Repair Status.
Hodel KP et al.
Molecular Cell, 2020
POLE proofreading defects: Contributions to mutagenesis and cancer.
Park VS et al.
Dna Repair, 2019
Adjuvant Treatment for POLE Proofreading Domain-Mutant Cancers: Sensitivity to Radiotherapy, Chemotherapy, and Nucleoside Analogues.
Van Gool IC et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2018
Explosive mutation accumulation triggered by heterozygous human Pol ε proofreading-deficiency is driven by suppression of mismatch repair.
Hodel KP et al.
Elife, 2018
The dominant role of proofreading exonuclease activity of replicative polymerase ε in cellular tolerance to cytarabine (Ara-C).
Tsuda M et al.
Oncotarget, 2017
Exonuclease mutations in DNA polymerase epsilon reveal replication strand specific mutation patterns and human origins of replication.
Shinbrot E et al.
Genome Research, 2014
DNA polymerase ε and its roles in genome stability.
Henninger EE et al.
Iubmb Life, 2014
Human Pol ε-dependent replication errors and the influence of mismatch repair on their correction.
Agbor AA et al.
Dna Repair, 2013