Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers

By W. Sakai, E. Swisher, B. Karlan, M. Agarwal, J. Higgins, C. Friedman, E. Villegas, C. Jacquemont, Daniel J. Farrugia, F. Couch and 2 more. Nature, 2008

1,086 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3544245aa96a4fbcc5104db756851ffc550a8c60

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Citations in the corpus

MMEJ repair of double-strand breaks (director’s cut): deleted sequences and alternative endings (2008, background): “Furthermore, a more complete understanding of the cellular contexts which favor MMEJ might serve to improve cancer treatments, as demonstrated by the potential role of MMEJ in chemotherapy-induced brca2 mutation reversion [78, 79 ].”
Cisplatin Resistance: A Cellular Self-Defense Mechanism Resulting from Multiple Epigenetic and Genetic Changes (2012, background): “Sakai et al. (2008, 2009) demonstrated secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated ovarian cancers, confirming that acquired resistance to cisplatin was due to secondary intragenic mutations in BRCA2 that restore the wild-type BRCA2 reading frame.”
PARP inhibition: PARP1 and beyond (2010, background): “gov/drugdictionary/?CdrID=39176">carboplatin can arise in BRCA1 - or BRCA2 -deficient cancer cells concomitant with the reactivation of these genes by secondary mutation”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “These tumors are defective in homologous recombination-mediated DNA repair and are particularly sensitive to DNA crosslinkers such as cisplatin (Sakai et al., 2008).”
How the fanconi anemia pathway guards the genome. (2009, background): “The downside, however, is that, probably owing to their lower accuracy of DNA repair, these cells accumulate secondary intragenic modifications that can lead to reversal of the BRCA2 mutation, allowing these cells to acquire crosslink resistance (43, 123).”
The DNA damage response and cancer therapy (2012, background): “In two studies, PARP-inhibitor resistance was caused by secondary mutations in the BRCA1 or BRCA2 genes themselve”
53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks (2010, positive): “More recently, it has been observed that Brca2-deficient tumors are capable of acquiring reversion mutations that enable resistance to chemotherapeutic agents (Edwards et al., 2008; Sakai et al., 2008).”
Tumor heterogeneity: causes and consequences (2009, background): “These tumors are deficient in homologous recombination-mediated DNA repair (HRR), which increases their genomic instability but makes them highly sensitive to platinum compounds and PARP (poly ADP ribose polymerase) inhibitors.”
Systems biology of cisplatin resistance: past, present and future (2014, background): “in breast carcinoma cells.(142) Mutations of this type not only have been associated with the resistance of ovarian carcinoma to platinum-based chemotherapy(142,143) but also appear”