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.
Original language | English (US) |
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Pages (from-to) | 1114-1122 |
Number of pages | 9 |
Journal | British journal of cancer |
Volume | 105 |
Issue number | 8 |
DOIs | |
State | Published - Oct 11 2011 |
Keywords
- BRCA1
- BRCA2
- DNA repair
- Poly (ADP-ribose) polymerases
- homologous recombination
ASJC Scopus subject areas
- Oncology
- Cancer Research