PARP inhibitors for BRCA1/2-mutated and sporadic ovarian cancer: current practice and future directions

British Journal of Cancer - open access

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PARP inhibitors for BRCA1/2-mutated and sporadic ovarian cancer: current practice and future directions

G E Konecny and R S Kristeleit

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Figure 1.

Role of PARP in DNA repair and main effects of PARP inhibitors. (A) Main DNA repair mechanisms, key pathway components and role of PARP1 for each pathway. (B) DNA single strand break repair by base excision repair. (C) Effect of PARP inhibition on DNA single and double strand break repair. AP, apurinic/apyrimidinic; ATM, ataxia telangiectasia; BER, base excision repair; DNA-PKcs, DNA-dependent protein kinase, catalytic subunit; DSB, double-strand break; FA, Fanconi anemia; FEN1, flap sructure-specific endonuclease 1; HR, homologous recombination; KU70 and KU80, make up the Ku heterodimer; MMEJ, microhomologymediated end joining; MRN, MRE11–RAD50–NBS1 protein complex; NBN, Nibrin; NHEJ, non-homologous end joining; PARP, poly (ADP-ribose) polymerase; PALB2, partner and localiser of BRC; PARPi, PARP inhibitor; RAD51, eukaryote gene of RAD51 protein family; SSB, single-strand break.
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Table 1 - PARP inhibitors under development.

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Table 2 - Most common AEs (any grade and grade 3) with olaparib treatment based on data from 2 large olaparib clinical trials. Shown are any grade AEs reported in at least 15% of patients or grade 3 AEs reported in at least 5% of patients.

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Table 3 - Clinical Trials of PARP inhibitors in ovarian cancer.

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