ReviewDNA repair2019
POLE proofreading defects: Contributions to mutagenesis and cancer.
Review in DNA repair, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.
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
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- Research progress on the role and mechanism of DNA damage repair in germ cell development.Frontiers in endocrinology · 2023Pooled it
- Ultra-mutated colorectal cancer patients with POLE driver mutations exhibit distinct clinical patterns.Cancer medicine · 2021Pooled it
- Interpreting the effects of DNA polymerase variants at the structural level.Molecular oncology · 2026Article
- Navigating Immunotherapy in a Kidney Transplant Recipient: A Case Report of POLE-Mutated Jejunal Adenocarcinoma.Cureus · 2026Article
- Role of POLE2/GINS1-mediated AKT/mTOR pathway in RCC autophagy, proliferation, and metastasis: evidences from bioinformatic, clinical, and experimental data.Apoptosis : an international journal on programmed cell death · 2026Article
- Selective Inhibition of Proofreading Exonucleases: The Central Role in Obesity-Associated Carcinogenesis.Current issues in molecular biology · 2026Review
- Review
- XPO1 R749Q Mutations Co-occur with POLE Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance.Cancer research · 2025Article
- Functions, interactions and prognostic role ofJournal of gynecologic oncology · 2025Article
- Immune Checkpoint Blockade Delays Cancer Development and Extends Survival in DNA Polymerase Mutator Syndromes.Cancer research · 2025Article
- A novel missense mutation c.1381T>C: p.(S461P) inFrontiers in oncology · 2025Article
- A novel patient-derived cutaneous melanoma cell line reveals key features of metastatic melanoma.Frontiers in oncology · 2025Article
- Molecular Classification of Endometrial Cancer and Its Impact on Therapy Selection.International journal of molecular sciences · 2024Review
- Deep learning for dual detection of microsatellite instability and POLE mutations in colorectal cancer histopathology.NPJ precision oncology · 2024Article
- POLE -related gene signature predicts prognosis, immune feature, and drug therapy in human endometrioid carcinoma.Heliyon · 2024Article
- POLE2 promotes osteosarcoma progression by enhancing the stability of CD44.Cell death discovery · 2024Article
- Exploring Co-occurring POLE Exonuclease and Non-exonuclease Domain Mutations and Their Impact on Tumor Mutagenicity.Cancer research communications · 2024Article
- SETD2 variation correlates with tumor mutational burden and MSI along with improved response to immunotherapy.BMC cancer · 2023Article
- Article
- Candidate variants in DNA replication and repair genes in early-onset renal cell carcinoma patients referred for germline testing.BMC genomics · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA polymerases are uniquely poised to contribute to the elevated mutation burdens seen in many human tumors. These mutations can arise through a number of different polymerase-dependent mechanisms, including intrinsic errors made using template DNA and precursor dNTPs free from chemical modifications, misinsertion events opposite chemically damaged template DNA or insertion events using modified nucleotides. While specific DNA repair polymerases have been known to contribute to tumorigenesis, the role of replication polymerases in mutagenesis in human disease has come into sharp focus over the last decade. This review describes how mutations in these replication DNA polymerases help to drive mutagenesis and tumor development, with particular attention to DNA polymerase epsilon. Recent studies using cancer genome sequencing, mutational signature analyses, yeast and mouse models, and the influence of mismatch repair on tumors with DNA polymerase mutations are discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.