ReviewClinical oncology (Royal College of Radiologists (Great Britain))2019
DNA Repair: Translation to the Clinic.
Review in Clinical oncology (Royal College of Radiologists (Great Britain)), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Prognostic, Predictive, and Clinical Relevance of DNA Damage Repair Alterations in Biliary Tract Cancers.Cancers · 2026Review
- Social context prevents heat hormetic effects against mutagens during fish development.FEBS letters · 2025Article
- Genomic characterization of chronic lymphocytic leukemia in patients of African ancestry.Blood cancer journal · 2025Article
- STK39-mediated amplification of γ-H2A.X promotes homologous recombination and contributes to PARP inhibitor resistance.Nucleic acids research · 2024Article
- Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition.NPJ precision oncology · 2024Article
- NUDT16 regulates CtIP PARylation to dictate homologous recombination repair.Nucleic acids research · 2024Article
- Association between polymorphisms of the DNA repair genes RAD51 and OGG1 and risk of cardiovascular disease.Molecular medicine reports · 2024Article
- Cellular and Molecular Biological Alterations after Photon, Proton, and Carbon Ions Irradiation in Human Chondrosarcoma Cells Linked with High-Quality Physics Data.International journal of molecular sciences · 2022Article
- Homologous Recombination Repair in Biliary Tract Cancers: A Prime Target for PARP Inhibition?Cancers · 2022Review
- Quantitative proteomic analysis of the lysine acetylome reveals diverse SIRT2 substrates.Scientific reports · 2022Article
- Dose Adjustment of Poly (ADP‑Ribose) Polymerase Inhibitors in Patients with Hepatic or Renal Impairment.Drug design, development and therapy · 2022Review
- Transcriptomic Responses ofFrontiers in cellular and infection microbiology · 2022Article
- Article
- Keap1 inhibition sensitizes head and neck squamous cell carcinoma cells to ionizing radiation via impaired non-homologous end joining and induced autophagy.Cell death & disease · 2020Article
- The Intermediate Filament Synemin Regulates Non-Homologous End Joining in an ATM-Dependent Manner.Cancers · 2020Article
- Epigenetic based synthetic lethal strategies in human cancers.Biomarker research · 2020Review
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
It has been well established that an accumulation of mutations in DNA, whether caused by external sources (e.g. ultraviolet light, radioactivity) or internal sources (e.g. metabolic by-products, such as reactive oxygen species), has the potential to cause a cell to undergo carcinogenesis and increase the risk for the development of cancer. Therefore, it is critically important for a cell to have the capacity to properly respond to and repair DNA damage as it occurs. The DNA damage response (DDR) describes a collection of DNA repair pathways that aid in the protection of genomic integrity by detecting myriad types of DNA damage and initiating the correct DNA repair pathway. In many instances, a deficiency in the DDR, whether inherited or spontaneously assumed, can increase the risk of carcinogenesis and ultimately tumorigenesis through the accumulation of mutations that fail to be properly repaired. Interestingly, although disruption of the DDR can lead to the initial genomic instability that can ultimately cause carcinogenesis, the DDR has also proven to be an invaluable target for anticancer drugs and therapies. Making matters more complicated, the DDR is also involved in the resistance to first-line cancer therapy. In this review, we will consider therapies already in use in the clinic and ongoing research into other avenues of treatment that target DNA repair pathways in cancer.
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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.