High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs

By S. Rottenberg, J. Jaspers, A. Kersbergen, Eline van der Burg, A. Nygren, Serge A. L. Zander, P. Derksen, M. de Bruin, J. Zevenhoven, A. Lau and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2008

962 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/774d0b467eeb38624efaf2101297d8abfaa42ff7

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Citations in the corpus

The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings (2011, background): “BRCA1 and BRCA2 defective tumours are intrinsically sensitive to PARP inhibitors, both in tumour models in vivo (Bryant et al., 2005; Evers et al., 2010; Farmer et al., 2005; Liu et al., 2007; Rottenberg et al., 2008) and in the clinic (Fong et al., 2009).”
Triple-negative breast cancer--current status and future directions. (2009, background): “Consequently, a number of clinical trials are currently being conducted with PARP inhibitors either alone or in combination with platinumbased chemotherapy, some of which have already provided promising results [148].”
The DNA damage response and cancer therapy (2012, background): “Other identified mechanisms of PARP-inhibitor response include the upregulation of genes that encode P-glycoprotein efflux pump”
A decade of clinical development of PARP inhibitors in perspective (2019, background): “Beyond mechanisms rewiring the DNA damage response, increased expression of ATP-binding cassette transporters, such as the P-glycoprotein efflux pump have been shown to reduce the efficacy of PARPi [84].”
Laying a trap to kill cancer cells: PARP inhibitors and their mechanisms of action (2016, methodology): “Initial data in vitro (34, 35) were followed by in vivo studies in BRCA knockout mice (36, 37) and then by clinical validation (38) with olaparib in patients with hereditary germline BRCA mutations.”
Thresholds for therapies: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2009 (2009, background): “BRCA1 mutations are associated with triple-negative phenotype, which require clinical evaluation of novel therapeutic approaches including poly (ADP-ribose) polymerase inhibitors and DNA-damaging agents [4, 5].”
Homologous recombination deficiency: Exploiting the fundamental vulnerability of ovarian cancer (2015, background): “Furthermore, resistance to PARPi could be reversed by coadministration of PgP inhibitors, arguing that upregulation of PgP may be a clinically relevant and druggable acquired mechanism of PARPi resistance (164, 165).”
Deconstructing the molecular portraits of breast cancer (2010, background): “The inhibition of PARP1 in this BRCA1 dysfunctional context leads to the accumulation of collapsed replication forks, DNA doublestrand breaks, and cell death (Rottenberg et al., 2008).”