PARP inhibitors for BRCA1/2-mutated and sporadic ovarian cancer: current practice and future directions Ovarian Cancer and Us OVARIAN CANCER and US Ovarian Cancer and Us

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Sunday, October 16, 2016

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



British Journal of Cancer - open access

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 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the author

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 3 - Clinical Trials of PARP inhibitors in ovarian cancer - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the author

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