Cediranib suppresses homology-directed DNA repair through down-regulation of BRCA1/2 and RAD51
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Cediranib directly suppresses homology-directed DNA repair in tumor cells and confers synthetic lethal vulnerability to PARP inhibitors.
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The combination of cediranib and olaparib induces lethality by suppressing DNA repair.
“The combination of cediranib and olaparib induces lethality by suppressing DNA repair.”
From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [103]
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Self-citation
- Authors
- Kaplan, A. R., Gueble, S. E., Liu, Y., Oeck, S., Kim, H., Yun, Z., & Glazer, P. M.
- Affiliations
- Yale University (US)
- Corresponding author
- Glazer, Peter M.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2019-05-15
- Volume
- 11
- Issue
- 492
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6626544
- OpenAlex
- W2946425279
- Cited by
- 158
- References
- 34
- Citations by year
- 2026: 14 · 2025: 15 · 2024: 21 · 2023: 23 · 2022: 17 · 2021: 29 · 2020: 31 · 2019: 8
- FWCI
- 8.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01ES005775, R35CA197574, R01CA178254, F30CA221065, T32GM007205)
- Topics
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Keywords
- cediranib, homology-directed repair, BRCA1, BRCA2, RAD51, synthetic lethality, olaparib, DNA repair inhibition, PARP inhibitor combination, tumor xenografts, myelosuppression
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Tumor Hypoxia, Animals, DNA Repair, Female, Humans, Indoles, Mice, Nude, Quinazolines, Down-Regulation, Gene Expression Regulation, Neoplastic, Receptors, Platelet-Derived Growth Factor, BRCA1 Protein, Xenograft Model Antitumor Assays, BRCA2 Protein, Vascular Endothelial Growth Factor Receptor-2, Cell Line, Tumor, E2F4 Transcription Factor, Rad51 Recombinase
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