ReviewNature reviews. Cancer2011
DNA polymerases and cancer.
Review in Nature reviews. Cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 340 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
340 citing papers in PubMed, 2 syntheses or guidelines pooled it, 617 citations in OpenAlex.
- A Meta-Analysis for Association of XRCC1, XRCC2 and XRCC3 Polymorphisms with Susceptibility to Thyroid Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021Pooled it
- Conservation and divergence of the p53 gene regulatory network between mice and humans.Oncogene · 2019Pooled it
- The polymerase milieu of human papillomavirus.Journal of virology · 2026Review
- Atomistic Simulations Decode the Mechanisms of DNA and RNA Processing Enzymes: Function through Motion.Accounts of chemical research · 2026Article
- Ionizing Radiation and Ultraviolet Light Irradiation-Associated DNA Damage Increasing Genomic Instability Risk.Cancer science · 2026Review
- Investigating the anticancer activity of eravacycline in pancreatic cancer via target-based deep learning and experimental validation.Briefings in bioinformatics · 2026Article
- Persistent interferon signaling and clonal expansion mark early events in DNA methylation damage-induced liver cancer.NAR cancer · 2026Article
- Multiplexed perturbation enables scalable pooled screens.Nature methods · 2026Article
- Article
- The DNA helicase HELQ promotes replication fork reversal in coordination with BRCA2- and FANCD2-mediated repair pathways.Nucleic acids research · 2026Article
- Pooled single-cell screen in colorectal cancer defines transcriptional modules linked to oncogenes.Molecular systems biology · 2026Article
- Article
- Machine learning and metabolic modeling-based identification of hypoxia-driven metabolic signatures in pediatric cancers.Frontiers in pharmacology · 2026Article
- Article
- Mitomycin C-induced DNA double-strand breaks are enhanced by catalytical inactivation of DNA polymerase κ in mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
- Persistent interferon signaling and clonal expansion mark early events in DNA methylation damage-induced liver cancer.bioRxiv : the preprint server for biology · 2025Article
- Compound Heterozygous Complete Loss-of-FunctionGenes · 2025Article
- Functional germline variants in DNA damage repair pathways are associated with altered survival in adults with glioma treated with temozolomide.Neuro-oncology · 2025Article
- Identifying Rare Germline Variants Associated with Metastatic Prostate Cancer Through an Extreme Phenotype Study.medRxiv : the preprint server for health sciences · 2025Article
- Expression of REV7 has prognostic significance in cervical cancer treated with intensity-modulated radiation therapy.Discover oncology · 2025Article
280 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
3 authors at 2 institutions in 1 country.
Funding
Abstract
There are 15 different DNA polymerases encoded in mammalian genomes, which are specialized for replication, repair or the tolerance of DNA damage. New evidence is emerging for lesion-specific and tissue-specific functions of DNA polymerases. Many point mutations that occur in cancer cells arise from the error-generating activities of DNA polymerases. However, the ability of some of these enzymes to bypass DNA damage may actually defend against chromosome instability in cells, and at least one DNA polymerase, Pol ζ, is a suppressor of spontaneous tumorigenesis. Because DNA polymerases can help cancer cells tolerate DNA damage, some of these enzymes might be viable targets for therapeutic strategies.
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.