ReviewFrontiers in oncology2015
Preventing Damage Limitation: Targeting DNA-PKcs and DNA Double-Strand Break Repair Pathways for Ovarian Cancer Therapy.
Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Roles of salt‑inducible kinases in cancer (Review).International journal of oncology · 2023Review
- Homologous repair deficiency-associated genes in invasive breast cancer revealed by WGCNA co-expression network analysis and genetic perturbation similarity analysis.Cell cycle (Georgetown, Tex.) · 2023Article
- An mTOR and DNA-PK dual inhibitor CC-115 hinders non-small cell lung cancer cell growth.Cell death discovery · 2022Article
- Difluoromethylornithine (DFMO) Enhances the Cytotoxicity of PARP Inhibition in Ovarian Cancer Cells.Medical sciences (Basel, Switzerland) · 2022Article
- DNA Repair Protein HELQ and XAB2 as Chemoresponse and Prognosis Biomarkers in Ascites Tumor Cells of High-Grade Serous Ovarian Cancer.Journal of oncology · 2022Article
- A Novel Salt Inducible Kinase 2 Inhibitor, ARN-3261, Sensitizes Ovarian Cancer Cell Lines and Xenografts to Carboplatin.Cancers · 2021Article
- NEAT1/miR-101-dependent Up-regulation of DNA-PKcs Enhances Malignant Behaviors of Pancreatic Ductal Adenocarcinoma Cells.Journal of Cancer · 2021Article
- Article
- Modulation of DNA double-strand break repair as a strategy to improve precise genome editing.Oncogene · 2020Review
- (S)-crizotinib reduces gastric cancer growth through oxidative DNA damage and triggers pro-survival akt signal.Cell death & disease · 2018Article
- Insight into the role of PIKK family members and NF-кB in DNAdamage-induced senescence and senescence-associated secretory phenotype of colon cancer cells.Cell death & disease · 2018Article
- Targeting DNA repair and replication stress in the treatment of ovarian cancer.International journal of clinical oncology · 2017Review
- Article
- Synergistic effects of a novel lipid-soluble extract fromOncology letters · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platinum-based chemotherapy is the cornerstone of ovarian cancer treatment, and its efficacy is dependent on the generation of DNA damage, with subsequent induction of apoptosis. Inappropriate or aberrant activation of the DNA damage response network is associated with resistance to platinum, and defects in DNA repair pathways play critical roles in determining patient response to chemotherapy. In ovarian cancer, tumor cell defects in homologous recombination - a repair pathway activated in response to double-strand DNA breaks (DSB) - are most commonly associated with platinum-sensitive disease. However, despite initial sensitivity, the emergence of resistance is frequent. Here, we review strategies for directly interfering with DNA repair pathways, with particular focus on direct inhibition of non-homologous end joining (NHEJ), another DSB repair pathway. DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is a core component of NHEJ and it has shown considerable promise as a chemosensitization target in numerous cancer types, including ovarian cancer where it functions to promote platinum-induced survival signaling, via AKT activation. The development of pharmacological inhibitors of DNA-PKcs is on-going, and clinic-ready agents offer real hope to patients with chemoresistant disease.
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