A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair.

By Alan Ashworth. Journal of Clinical Oncology, 2008

859 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/89fe45f158c129a4ef77c5dcbeba09f7e7f39e3d

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Citations in the corpus

Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. (2009, neutral): “Breast 9 (15) Colorectal 8 ( 13 ) Melanoma 4 (7)”
Triple-negative breast cancer: disease entity or title of convenience? (2010, background): “and susceptibility to chemotherapy and other agents which target DNA repair by poly (ADP-ribose) polymerase (PARP) inhibition”
Laying a trap to kill cancer cells: PARP inhibitors and their mechanisms of action (2016, background): “1G), cancer cells with homologous recombination repair deficiencies (HRDs), such as BRCA loss-of-function mutations, would only have low-fidelity repair pathways to fall back on, resulting in an increase in genomic instability, ultimately leading to tumor-specific cell death (39).”
Recent Progress in the Diagnosis and Treatment of Ovarian Cancer (2011, background): “Because PARP is critical to the process of single-strand DNA repair, PARP inhibitors could prevent cells with aberrant BRCA function from repairing chemotherapy-induced DNA damage, thus increasing cytotoxicity.(126) In a phase 1 trial of the oral PARP inhibitor AZD2281 (olaparib), 21 of 46 (46%) ova”
Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors (2009, positive): “The exquisite sensitivity of BRCA1 or BRCA2 mutant cells to PARP inhibitors (PARPi) forms the rationale behind clinical trials that are now assessing the potential of these agents (Ashworth, 2008).”
Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. (2010, background): “In HR DNA repair defective cells, PARP inhibition results in unrepaired DNA single-strand and double-strand breaks and eventual cell death.(13) Cancer cell sensitivity and resistance to both PARP inhibition and platinum have been associated with loss and restoration of HR DNA repair, respectively, i”