ReviewInternational journal of clinical oncology2017
Targeting DNA repair and replication stress in the treatment of ovarian cancer.
Review in International journal of clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 81 citations in OpenAlex.
- Clinicopathological and functional evaluation of replication protein A in epithelial ovarian cancers: A target validation study.Translational oncology · 2026Article
- Ubiquitin-related gene markers predict immunotherapy response and prognosis in patients with epithelial ovarian carcinoma.Scientific reports · 2024Article
- Radiosensitization of Osteosarcoma Cells Using the PARP Inhibitor Olaparib Combined with X-rays or Carbon Ions.Journal of Cancer · 2024Article
- DNA Double-Strand Break Repair Inhibitors: YU238259, A12B4C3 and DDRI-18 Overcome the Cisplatin Resistance in Human Ovarian Cancer Cells, but Not under Hypoxia Conditions.Current issues in molecular biology · 2023Article
- Altered expression of the L-arginine/nitric oxide pathway in ovarian cancer: metabolic biomarkers and biological implications.BMC cancer · 2023Article
- Schlafen 11 (SLFN11) Kills Cancer Cells Undergoing Unscheduled Re-replication.Molecular cancer therapeutics · 2023Article
- Enhanced phosphorylation of c-Jun by cisplatin treatment as a potential predictive biomarker for cisplatin response in combination with patient-derived tumor organoids.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Article
- Reconsidering the mechanisms of action of PARP inhibitors based on clinical outcomes.Cancer science · 2022Review
- Construction of miRNA-lncRNA-mRNA co-expression network affecting EMT-mediated cisplatin resistance in ovarian cancer.Journal of cellular and molecular medicine · 2022Article
- Topoisomerase II poisons inhibit vertebrate DNA replication through distinct mechanisms.The EMBO journal · 2022Article
- PARP inhibitors trap PARP2 and alter the mode of recruitment of PARP2 at DNA damage sites.Nucleic acids research · 2022Article
- Effects of Wee1 inhibitor adavosertib on patient-derived high-grade serous ovarian cancer cells are multiple and independent of homologous recombination status.Frontiers in oncology · 2022Article
- Identification of a signature of evolutionarily conserved stress-induced mutagenesis in cancer.Frontiers in genetics · 2022Article
- NovelFrontiers in oncology · 2022Review
- Development of poly(ADP-ribose) polymerase inhibitor and immunotherapy combinations: progress, pitfalls, and promises.Trends in cancer · 2021Review
- Enhanced Efficacy of Combined Therapy with Checkpoint Kinase 1 Inhibitor and Rucaparib via Regulation of Rad51 Expression in BRCA Wild-Type Epithelial Ovarian Cancer Cells.Cancer research and treatment · 2021Article
- PARP1-Inhibition Sensitizes Cervical Cancer Cell Lines for Chemoradiation and Thermoradiation.Cancers · 2021Article
- CDCA8, targeted by MYBL2, promotes malignant progression and olaparib insensitivity in ovarian cancer.American journal of cancer research · 2021Article
- Influence of humanistic care based on Carolina care model for ovarian cancer patients on postoperative recovery and quality of life.American journal of translational research · 2021Article
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
Approximately half of high-grade serous epithelial ovarian cancers incur alterations in genes of homologous recombination (BRCA1, BRCA2, RAD51C, Fanconi anemia genes), and the rest incur alterations in other DNA repair pathways at high frequencies. Such cancer-specific gene alterations can confer selective sensitivity to DNA damaging agents such as cisplatin and carboplatin, topotecan, etoposide, doxorubicin, and gemcitabine. Originally presumed to inhibit DNA repair, PARP inhibitors that have recently been approved by the FDA for the treatment of advanced ovarian cancer also act as DNA damaging agents by inducing PARP-DNA complexes. These DNA damaging agents induce different types of DNA lesions that require various DNA repair genes for the repair, but commonly induce replication fork slowing or stalling, also referred to as replication stress. Replication stress activates DNA repair checkpoint proteins (ATR, CHK1), which prevent further DNA damage. Hence, targeting DNA repair genes or DNA repair checkpoint genes augments the anti-tumor activity of DNA damaging agents. This review describes the rational basis for using DNA repair and DNA repair checkpoint inhibitors as single agents. The review also presents the strategies combining these inhibitors with DNA damaging agents for ovarian cancer therapy based on specific gene alterations.
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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.