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Cited by 320

The DOI matches its Crossref record; 220 of the 220 references it cites were found in a registry or an index.

The role of PARP in DNA repair and its therapeutic exploitation

Open access
Javle, M, Curtin, N J·2011·British Journal of Cancer

Abstract

Historically, PARP inhibitors (PARPi) were developed to potentiate the cytotoxic effect of certain chemotherapeutic agents and are currently being investigated in combination with chemotherapy in diverse cancer types. These agents are also radiosensitisers and clinical trials of PARPi with concurrent radiation are required. It has long been recognised that defective DNA repair pathways lead to tumour susceptibility. Recent studies indicate that tumour cells with defective homologous recombination (HR) repair pathways, the classic example being BRCA mutations, are exquisitely sensitive to PARPi. Defects in HR are not restricted to BRCA-associated tumours and other cancer types may be enriched for HR defects and hence susceptible to PARP inhibition. The identification of predictive markers for sensitivity to PARP inhibition is a priority area for research.

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Metadata

Authors
Javle, M., & Curtin, N. J.
Venue
British Journal of Cancer
Published
2011-10
Volume
105
Issue
8
Pages
1114-1122
ISSN
  • 0007-0920 (ISSN-L)
  • 1532-1827
OpenAlex
W2124092811
Cited by
320
References
220
FWCI
9.93
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: The role of PARP in DNA repair and its therapeutic exploitation. https://app.cochat.ai/papers/10.1038/bjc.2011.382
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Javle, M., & Curtin, N. J. (2011). The role of PARP in DNA repair and its therapeutic exploitation. British Journal of Cancer. https://doi.org/10.1038/bjc.2011.382

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.