ArticleBiochemical Society transactions2023
Targeting the DNA damage response for cancer therapy.
Article in Biochemical Society transactions, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 41 citations in OpenAlex.
- Trial
- The DNA damage response and cancer immunotherapy.Nature reviews. Cancer · 2026Review
- Primary carcinosarcoma of the uterine cervix with somatic mutations of theInternational cancer conference journal · 2025Article
- Review
- Defective homologous recombination and genomic instability predict increased responsiveness to carbon ion radiotherapy in pancreatic cancer.NPJ precision oncology · 2025Article
- A Site-Specific Click Chemistry Approach to Di-Ubiquitylate H1 Variants Reveals Position-Dependent Stimulation of the DNA Repair Protein RNF168.Angewandte Chemie (International ed. in English) · 2024Article
- Quantitation of the DNA-dependent protein kinase inhibitor peposertib (M3814) and metabolite in human plasma by LC-MS/MS.Biomedical chromatography : BMC · 2024Article
- Structure-based discovery of first inhibitors targeting the helicase activity of human PIF1.Nucleic acids research · 2024Article
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- Prediction of homologous recombination deficiency identifies colorectal tumors sensitive to PARP inhibition.NPJ precision oncology · 2024Article
- Review
- TIPRL1 and its ATM-dependent phosphorylation promote radiotherapy resistance in head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Quantitative, titratable and high-throughput reporter assays to measure DNA double strand break repair activity in cells.Nucleic acids research · 2024Article
- Targeting ATR Pathway in Solid Tumors: Evidence of Improving Therapeutic Outcomes.International journal of molecular sciences · 2024Review
- Paradigm Shift: A Comprehensive Review of Ovarian Cancer Management in an Era of Advancements.International journal of molecular sciences · 2024Review
- Combinatorial targeting of telomerase and DNA-PK induces synergistic apoptotic effects against Pre-B acute lymphoblastic leukemia cells.Molecular biology reports · 2024Article
- The future of cancer treatment: combining radiotherapy with immunotherapy.Frontiers in molecular biosciences · 2024Review
- DNA damage response inhibitors enhance tumour treating fields (TTFields) potency in glioma stem-like cells.British journal of cancer · 2023Article
- Microsatellite instability states serve as predictive biomarkers for tumors chemotherapy sensitivity.iScience · 2023Article
- Impaired DNA double-strand break repair and effective radiosensitization of HPV-negative HNSCC cell lines through combined inhibition of PARP and Wee1.Clinical and translational radiation oncology · 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA damage response (DDR) is an elegant system, coordinating DNA repair with cell cycle checkpoints, that evolved to protect living organisms from the otherwise fatal levels of DNA damage inflicted by endogenous and environmental sources. Since many agents used to treat cancer; radiotherapy and cytotoxic chemotherapy, work by damaging DNA the DDR represents a mechanism of resistance. The original rational for the development of drugs to inhibit the DDR was to overcome this mechanism of resistance but clinical studies using this approach have not led to improvements in the therapeutic index. A more exciting approach is to exploit cancer-specific defects in the DDR, that represent vulnerabilities in the tumour and an opportunity to selectively target the tumour. PARP inhibitors (PARPi) selectively kill homologous recombination repair defective (HRD, e.g. through BRCA mutation) cells. This approach has proven successful clinically and there are now six PARPi approved for cancer therapy. Drugs targeting other aspects of the DDR are under pre-clinical and clinical evaluation as monotherapy agents and in combination studies. For this promising approach to cancer therapy to be fully realised reliable biomarkers are needed to identify tumours with the exploitable defect for monotherapy applications. The possibility that some combinations may result in toxicity to normal tissues also needs to be considered. A brief overview of the DDR, the development of inhibitors targeting the DDR and the current clinical status of such drugs is described here.
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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.