ArticleTranslational cancer research2017
Repurposing DNA repair factors to eradicate tumor cells upon radiotherapy.
Article in Translational cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Analysis of the TCRβ repertoire characteristics when combining radiotherapy and immunotherapy in cancer.Oncology letters · 2026Article
- Functional Profiling of DNA Repair Pathways in Lung Cancer Patients Uncovers Radiotherapy-Induced and Cancer-Associated Alterations in Oxidative Lesion Repair.medRxiv : the preprint server for health sciences · 2026Article
- Radioprotective Potential of a Polyphenol-Rich Extract Blend: Preclinical Evaluation in Female Balb/c Mice Exposed to Ionizing Radiation.International journal of molecular sciences · 2025Article
- Machine learning-based screening and molecular simulations for discovering novel PARP-1 inhibitors targeting DNA repair mechanisms for breast cancer therapy.Molecular diversity · 2025Article
- Investigation of the Molecular Mechanisms of Paraoxonase-2 Mediated Radiotherapy and Chemotherapy Resistance in Oral Squamous Cell Carcinoma.Clinical and translational science · 2025Review
- Microbiota-mediated modulation of radiosensitivity: mechanisms and therapeutic prospects of oral and gut microbiota, metabolites, and probiotics.Frontiers in microbiology · 2025Review
- Role of Oxidative Stress Signaling, Nrf2, on Survival and Stemness of Human Adipose-Derived Stem Cells Exposed to X-rays, Protons and Carbon Ions.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- Review
- The radiation response measurement of a single and multiple cell ionization of neuroblastoma cells by infrared laser trap.Journal of radiation research · 2023Article
- Photon- and Proton-Mediated Biological Effects: What Has Been Learned?Life (Basel, Switzerland) · 2022Review
- PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy.Cell & bioscience · 2022Article
- Inhibition of USP28 overcomes Cisplatin-resistance of squamous tumors by suppression of the Fanconi anemia pathway.Cell death and differentiation · 2022Article
- Review
- Radiotherapy-immunotherapy combinations - perspectives and challenges.Molecular oncology · 2020Review
- Article
- Cellular Stress Responses in Radiotherapy.Cells · 2019Review
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- Molecular Signaling in Response to Charged Particle Exposures and its Importance in Particle Therapy.International journal of particle therapy · 2018Review
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.
Funding
Abstract
Cancer is the leading cause of death worldwide. Almost 50% of all cancer patients undergo radiation therapy (RT) during treatment, with varying success. The main goal of RT is to kill tumor cells by damaging their DNA irreversibly while sparing the surrounding normal tissue. The outcome of RT is often determined by how tumors recognize and repair their damaged DNA. A growing body of evidence suggests that tumors often show abnormal expression of DNA double-strand break (DSB) repair genes that are absent from normal cells. Defects in a specific DNA repair pathway make tumor cells overly dependent on alternative or backup pathways to repair their damaged DNA. These tumor cell-specific abnormalities in the DNA damage response (DDR) machinery can potentially be used as biomarkers for treatment outcomes or as targets for sensitization to ionizing radiation (IR). An improved understanding of genetic or epigenetic alterations in the DNA repair pathways specific to cancer cells has paved the way for new treatments that combine pharmacological exploitation of tumor-specific molecular vulnerabilities with IR. Inhibiting DNA repair pathways has the potential to greatly enhance the therapeutic ratio of RT. In this review, we will discuss DNA repair pathways in active cells and how these pathways are deregulated in tumors. We will also describe the impact of targeting cancer-specific aberrations in the DDR as a treatment strategy to improve the efficacy of RT. Finally, we will address the current roadblocks and future prospects of these approaches.
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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.