ReviewEuropean journal of pharmacology2009
Impaired DNA damage response--an Achilles' heel sensitizing cancer to chemotherapy and radiotherapy.
Review in European journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 77 citations in OpenAlex.
- Breaking the Balance: Baseline Oxidative Stress and DNA Repair Capacity in Multiple Myeloma Therapy.Cancers · 2026Article
- HMGB1 Assists in Overcoming Cisplatin Resistance in Chemoresistant Human Ovarian Cancer Cells.Molecular carcinogenesis · 2026Article
- A new strategy for the treatment of advanced ovarian cancer: utilizing nanotechnology to regulate the tumor microenvironment.Frontiers in immunology · 2025Review
- Long noncoding RNA TUG1 promotes cisplatin resistance in ovarian cancer via upregulation of DNA polymerase eta.Cancer science · 2024Article
- DNA Damage and Its Role in Cancer Therapeutics.International journal of molecular sciences · 2023Review
- DNA Damage Response Alterations in Ovarian Cancer: From Molecular Mechanisms to Therapeutic Opportunities.Cancers · 2023Review
- Comparative analysis of chlorambucil-induced DNA lesion formation and repair in a spectrum of different human cell systems.Toxicology reports · 2023Article
- Nanotherapeutic Intervention in Photodynamic Therapy for Cancer.ACS omega · 2022Review
- HPV Enhances HNSCC Chemosensitization by Inhibiting SERPINB3 Expression to Disrupt the Fanconi Anemia Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- cGAS Regulates the Radioresistance of Human Head and Neck Squamous Cell Carcinoma Cells.Cells · 2022Article
- Role of Circulating Biomarkers in Platinum-Resistant Ovarian Cancer.International journal of molecular sciences · 2021Review
- Targeting DNA Damage Response and Repair to Enhance Therapeutic Index in Cisplatin-Based Cancer Treatment.International journal of molecular sciences · 2021Review
- Targeting DNA Damage Response Pathway in Ovarian Clear Cell Carcinoma.Frontiers in oncology · 2021Review
- Synthesis of newRSC advances · 2020Article
- Review
- Overcoming hypoxia-induced tumor radioresistance in non-small cell lung cancer by targeting DNA-dependent protein kinase in combination with carbon ion irradiation.Radiation oncology (London, England) · 2017Article
- Sensitization strategies in lung cancer.Oncology letters · 2016Article
- Article
- NRAGE is involved in homologous recombination repair to resist the DNA-damaging chemotherapy and composes a ternary complex with RNF8-BARD1 to promote cell survival in squamous esophageal tumorigenesis.Cell death and differentiation · 2016Article
- Chemical Reactivity Window Determines Prodrug Efficiency toward Glutathione Transferase Overexpressing Cancer Cells.Molecular pharmaceutics · 2016Article
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 2 countries.
Funding
Abstract
Despite the progress in targeting particular molecular abnormalities specific to different cancers (targeted therapy), chemo- and radiotherapies are still the most effective of all anticancer modalities. Induction of DNA damage and inhibition of cell proliferation are the objects of most chemotherapeutic agents and radiation. Their effectiveness was initially thought to be due to the high rate of proliferation of cancer cells. However, normal cell proliferation rate in some tissues often exceeds that of curable tumors. Most tumors have impaired DNA damage response (DDR) and the evidence is forthcoming that this confers sensitivity to chemo- or radiotherapy. DDR is a complex set of events which elicits a plethora of molecular interactions engaging signaling pathways designed to: (a) halt cell cycle progression and division to prevent transfer of DNA damage to progeny cells; (b) increase the accessibility of the damaged sites to the DNA repair machinery; (c) engage DNA repair mechanisms and (d) activate the apoptotic pathway when DNA cannot be successfully repaired. A defective DDR makes cancer cells unable to effectively stop cell cycle progression, engage in DNA repair and/or trigger the apoptotic program when treated with DNA damaging drugs. With continued exposure to the drug, such cells accumulate DNA damage which leads to their reproductive death that may have features of cell senescence. Cancers with nonfunctional BRCA1 and BRCA2 are particularly sensitive to combined treatment with DNA damaging drugs and inhibitors of poly(ADP-ribose) polymerase. Antitumor strategies are being designed to treat cancers having particular defects in their DDR, concurrent with protecting normal cells.
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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.