Abstract
Somatic or germline mutations in genes regulating DNA damage repair have been noted in around 20% of patients with advanced prostate cancer. Poly-ADP-ribose polymerase (PARP) inhibitors have shown encouraging efficacy in prostate cancer patients with DNA repair mutations. Two PARP inhibitors, olaparib, and rucaparib have recently received FDA approval for treatment of patients with advanced castration-resistant prostate cancer (CRPC), while several trials with other PARP inhibitors are ongoing. Here, we briefly summarize the current data supporting the efficacy of PARP inhibitors in advanced CRPC.
Keywords:
BRCA; Castration-resistant prostate cancer; PARP inhibitor; Prostate cancer; Targeted therapy.
Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.
MeSH terms
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Antineoplastic Combined Chemotherapy Protocols / pharmacology
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use*
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Biomarkers, Tumor / genetics*
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Clinical Decision-Making
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DNA Repair / drug effects
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Drug Approval
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Humans
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Indoles / pharmacology
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Indoles / therapeutic use
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Male
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Patient Selection
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Phthalazines / pharmacology
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Phthalazines / therapeutic use
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Piperazines / pharmacology
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Piperazines / therapeutic use
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Poly(ADP-ribose) Polymerase Inhibitors / pharmacology
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Poly(ADP-ribose) Polymerase Inhibitors / therapeutic use*
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Progression-Free Survival
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Prostatic Neoplasms, Castration-Resistant / drug therapy*
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Prostatic Neoplasms, Castration-Resistant / genetics
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Prostatic Neoplasms, Castration-Resistant / mortality
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Randomized Controlled Trials as Topic
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Synthetic Lethal Mutations / drug effects
Substances
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Biomarkers, Tumor
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Indoles
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Phthalazines
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Piperazines
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Poly(ADP-ribose) Polymerase Inhibitors
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rucaparib
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olaparib