ReviewDNA repair2017
Replicative DNA polymerase defects in human cancers: Consequences, mechanisms, and implications for therapy.
Review in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 110 citations in OpenAlex.
- Genome-wide CRISPR screens identify the EXO1-CAF-1 pathway suppressing R-loop-associated DNA damage.Nucleic acids research · 2026Article
- Cancer histone mutations impact protein binding and DNA repair with possible links to genomic instability.Nucleic acids research · 2025Article
- Comprehensive Analysis of Human Colorectal Cancers Harboring Polymerase Epsilon Mutations.International journal of molecular sciences · 2025Article
- Molecular subtyping of endometrial cancer via a simplified one-step NGS classifier, ARID1A and ZFHX4 mutations help further subclassify CNL/MSI-H patients.Diagnostic pathology · 2025Article
- When do the pathological signs become evident? Study of human mesenchymal stem cells in MDPL syndrome.Aging · 2024Article
- Human DNA polymerase ε is a source of C>T mutations at CpG dinucleotides.Nature genetics · 2024Article
- Effects of PCNA Stability on the Formation of Mutations.International journal of molecular sciences · 2024Article
- CSCO guidelines for colorectal cancer version 2024: Updates and discussions.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- USP1-dependent nucleolytic expansion of PRIMPOL-generated nascent DNA strand discontinuities during replication stress.Nucleic acids research · 2024Article
- Optimizing Design of Genomics Studies for Clonal Evolution Analysis.bioRxiv : the preprint server for biology · 2024Article
- DNA polymerase ε and δ variants drive mutagenesis in polypurine tracts in human tumors.Cell reports · 2024Article
- The P286R mutation of DNA polymerase ε activates cancer-cell-intrinsic immunity and suppresses endometrial tumorigenesis via the cGAS-STING pathway.Cell death & disease · 2024Article
- Optimizing design of genomics studies for clonal evolution analysis.Bioinformatics advances · 2024Article
- A simple bypass assay for DNA polymerases shows that cancer-associated hypermutating variants exhibit differences in vitro.The FEBS journal · 2023Article
- Recommendations for the classification of germline variants in the exonuclease domain of POLE and POLD1.Genome medicine · 2023Article
- Cancer driver mutations: predictions and reality.Trends in molecular medicine · 2023Review
- Dynamic basis for dA•dGTP and dA•d8OGTP misincorporation via Hoogsteen base pairs.Nature chemical biology · 2023Article
- Article
- Candidate variants in DNA replication and repair genes in early-onset renal cell carcinoma patients referred for germline testing.BMC genomics · 2023Article
- The importance of nuclear RAGE-Mcm2 axis in diabetes or cancer-associated replication stress.Nucleic acids research · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The fidelity of DNA replication relies on three error avoidance mechanisms acting in series: nucleotide selectivity of replicative DNA polymerases, exonucleolytic proofreading, and post-replicative DNA mismatch repair (MMR). MMR defects are well known to be associated with increased cancer incidence. Due to advances in DNA sequencing technologies, the past several years have witnessed a long-predicted discovery of replicative DNA polymerase defects in sporadic and hereditary human cancers. The polymerase mutations preferentially affect conserved amino acid residues in the exonuclease domain and occur in tumors with an extremely high mutation load. Thus, a concept has formed that defective proofreading of replication errors triggers the development of these tumors. Recent studies of the most common DNA polymerase variants, however, suggested that their pathogenicity may be determined by functional alterations other than loss of proofreading. In this review, we summarize our current understanding of the consequences of DNA polymerase mutations in cancers and the mechanisms of their mutator effects. We also discuss likely explanations for a high recurrence of some but not other polymerase variants and new ideas for therapeutic interventions emerging from the mechanistic studies.
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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.