Synthetic lethality of PARP inhibition in cancers lacking BRCA1 and BRCA2 mutations
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Utilizing the concept of synthetic lethality has provided new opportunities for the development of targeted therapies, by allowing the targeting of loss of function genetic aberrations. In cancer cells with BRCA1 or BRCA2 loss of function, which harbor deficiency of DNA repair by homologous recombination, inhibition of PARP1 enzymatic activity leads to an accumulation of single strand breaks that are converted to double strand breaks but cannot be repaired by homologous recombination. Inhibition of PARP has therefore been advanced as a novel targeted therapy for cancers harboring BRCA1/2 mutations. Preclinical and preliminary clinical evidence, however, suggests a potentially broader scope for PARP inhibitors. Loss of function of various proteins involved in double strand break repair other than BRCA1/2 has been suggested to be synthetically lethal with PARP inhibition. Inactivation of these genes has been reported in a subset of human cancers and might therefore constitute predictive biomarkers for PARP inhibition. Here we discuss the evidence that the clinical use of PARP inhibition may be broader than targeting of cancers in BRCA1/2 germ-line mutation carriers.
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Tumors with defects in homologous recombination repair are responsive to PARP inhibitors, functioning in a synthetic lethal manner to inhibit repair of single strand breaks via base excision repair.
“Tumors with defects in HRR are responsive to poly adenosine diphosphate-ribose polymerase inhibitors (PARPis), functioning in a synthetic lethal manner to inhibit repair of single strand breaks via the base excision repair pathway (Dedes et al., 2011).”
From Three-dimensional modelling of ovarian cancer: from cell lines to organoids for discovery and personalized medicine (2022) · cites this paper as Dedes et al., 2011
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Collateral lethality: a new therapeutic strategy in oncology
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- Authors
- Dedes, K. J., Wilkerson, P. M., Wetterskog, D., Weigelt, B., Ashworth, A., & Reis-Filho, J. S.
- Affiliations
- Institute of Cancer Research (GB)
- Corresponding author
- Reis-Filho, Jorge S.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2011-04-15
- Volume
- 10
- Issue
- 8
- Pages
- 1192-1199
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC3117132
- OpenAlex
- W1975307022
- Cited by
- 191
- References
- 97
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 12 · 2023: 17 · 2022: 12 · 2021: 8 · 2020: 10 · 2019: 13 · 2018: 8 · 2017: 14 · 2016: 12 · 2015: 11 · 2014: 18 · 2013: 12 · 2012: 19
- FWCI
- 8.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Science Foundation
- Breast Cancer Research Foundation
- Wellcome Trust
- Cancer Research UK
- Breast Cancer Campaign
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Stand Up To Cancer
- Topics
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- synthetic lethality, PARP inhibitors, BRCA1, BRCA2, homologous recombination deficiency, DNA double-strand break repair, targeted cancer therapy, predictive biomarkers, loss-of-function mutations
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Animals, Antineoplastic Agents, Clinical Trials as Topic, Disease Models, Animal, DNA Repair, Enzyme Inhibitors, Epistasis, Genetic, Female, Humans, Male, Neoplasms, Poly(ADP-ribose) Polymerases, Recombination, Genetic, Gene Expression, Germ-Line Mutation, Mice, Knockout, DNA Methylation, BRCA1 Protein, BRCA2 Protein, Mice, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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