ReviewBritish journal of pharmacology2013
Inhibiting the DNA damage response as a therapeutic manoeuvre in cancer.
Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 75 citations in OpenAlex.
- Phase 2 Study of Talazoparib in Patients With Homologous Recombination Repair-Deficient Squamous Cell Lung Cancer: Lung-MAP Substudy S1400G.Clinical lung cancer · 2021Trial
- ROS-Induced DNA Damage Enhances Sensitivity to PARP Inhibition in HSC3 and SCC25 Head and Neck Squamous Cell Carcinoma Cell Lines.Current issues in molecular biology · 2026Article
- Ruthenium(ii) polypyridyl complexes and the DNA damage response: mechanisms and therapeutic implications.RSC medicinal chemistry · 2026Review
- Resveratrol potentiates chemotherapeutic efficacy of olaparib in MCF7 human breast cancer cells by inducing apoptosis.Irish journal of medical science · 2026Article
- Translational Aspects of DNA Damage Repair in Optimizing Cancer Chemotherapy.Advanced genetics (Hoboken, N.J.) · 2025Review
- Post-translational modifications of SOG1 enable dynamic control of plant DNA damage response.Science advances · 2025Article
- Cytosolic Phospholipase A2 Determines Intercellular Heterogeneity of Stress Granules and Chemotherapy Response.Cancer discovery · 2025Article
- Identifying active and inhibitor-resistant MGMT variants for gene therapy.American journal of human genetics · 2025Article
- Bypass of Methoxyamine-Adducted Abasic Sites by Eukaryotic Translesion DNA Polymerases.International journal of molecular sciences · 2025Article
- Targeted radioligand therapy: physics and biology, internal dosimetry and other practical aspects duringTheranostics · 2025Review
- Integration of scRNA and bulk RNA-sequence to construct the 5-gene molecular prognostic model based on the heterogeneity of thyroid carcinoma endothelial cell.Acta biochimica et biophysica Sinica · 2024Article
- DNA damage response-related ncRNAs as regulators of therapy resistance in cancer.Frontiers in pharmacology · 2024Review
- Article
- Review
- DNA Damage Response Mechanisms in Head and Neck Cancer: Significant Implications for Therapy and Survival.International journal of molecular sciences · 2023Review
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022Review
- Article
- Impact of Non-Coding RNAs on Chemotherapeutic Resistance in Oral Cancer.Biomolecules · 2022Review
- Anti-cancer immune responses to DNA damage response inhibitors: Molecular mechanisms and progress toward clinical translation.Frontiers in oncology · 2022Review
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
Abstract
unlabelledThe DNA damage response (DDR), consisting of an orchestrated network of proteins effecting repair and signalling to cell cycle arrest, to allow time to repair, is essential for cell viability and to prevent DNA damage being passed on to daughter cells. The DDR is dysregulated in cancer with some pathways up-regulated and others down-regulated or lost. Up-regulated pathways can confer resistance to anti-cancer DNA damaging agents. Therefore, inhibitors of key components of these pathways have the potential to prevent this therapeutic resistance. Conversely, defects in a particular DDR pathway may lead to dependence on a complementary pathway. Inhibition of this complementary pathway may result in tumour-specific cell killing. Thus, inhibitors of the DDR have the potential to increase the efficacy of DNA damaging chemotherapy and radiotherapy and have single-agent activity against tumours with a specific DDR defect. This review describes the compounds that have been designed to inhibit specific DDR targets and summarizes the pre-clinical and clinical evaluation of these inhibitors of DNA damage signalling and repair. LINKED ARTICLES: This article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2013.169.issue-8.
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.