PARP Inhibitors Display Differential Efficacy in Models of BRCA Mutant High-Grade Serous Ovarian Cancer
Open accessAbstract
Several poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors are now in clinical use for tumours with defects in BReast CAncer genes BRCA1 or BRCA2 that result in deficient homologous recombination repair (HRR). Use of olaparib, niraparib or rucaparib for the treatment of high-grade serous ovarian cancer, including in the maintenance setting, has extended both progression free and overall survival for women with this malignancy. While different PARP inhibitors (PARPis) are mechanistically similar, differences are apparent in their chemical structures, toxicity profiles, PARP trapping abilities and polypharmacological landscapes. We have treated ovarian cancer cell line models of known BRCA status, including the paired cell lines PEO1 and PEO4, and UWB1.289 and UWB1.289+BRCA1, with five PARPis (olaparib, niraparib, rucaparib, talazoparib and veliparib) and observed differences between PARPis in both cell viability and cell survival. A cell line model of acquired resistance to veliparib showed increased resistance to the other four PARPis tested, suggesting that acquired resistance to one PARPi may not be able to be rescued by another. Lastly, as a proof of principle, HRR proficient ovarian cancer cells were sensitised to PARPis by depletion of BRCA1. In the future, guidelines will need to emerge to assist clinicians in matching specific PARPis to specific patients and tumours.
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Functional analyses, alongside molecular assays, are required to confirm the predicted response of women with ovarian cancer to PARP inhibitors such as olaparib, niraparib and rucaparib.
“Functional analyses, alongside molecular assays, are required to confirm the predicted response of women with ovarian cancer to PARPis such as the FDA-approved drugs olaparib, niraparib and rucaparib (Dickson et al., 2021; Lee et al., 2021; Valabrega et al., 2021).”
From Three-dimensional modelling of ovarian cancer: from cell lines to organoids for discovery and personalized medicine (2022) · cites this paper as Dickson et al., 2021
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- Authors
- Dickson, K.-A., Xie, T., Evenhuis, C., Ma, Y., & Marsh, D. J.
- Affiliations
- University of Technology Sydney (AU)
- Corresponding author
- Marsh, Deborah J.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2021-08-07
- Volume
- 22
- Issue
- 16
- Pages
- 8506
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC8395221
- OpenAlex
- W3192400176
- Cited by
- 11
- References
- 59
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 5
- FWCI
- 0.82
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UTS ePRESS (University of Technology Sydney) (submittedVersion, other-oa)
- Funders
- University of Technology Sydney
- Topics
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Reproductive Medicine › Ovarian cancer diagnosis and treatment
- Keywords
- PARP inhibitors, high-grade serous ovarian cancer, BRCA1, BRCA2, homologous recombination deficiency, olaparib, niraparib, rucaparib, talazoparib, veliparib, acquired drug resistance, PARP trapping, maintenance therapy
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Female, Humans, Models, Biological, Mutation, Ovarian Neoplasms, BRCA1 Protein, BRCA2 Protein, Cell Line, Tumor
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