Whole–genome characterization of chemoresistant ovarian cancer

By A. Patch, E. Christie, D. Etemadmoghadam, D. Garsed, J. George, S. Fereday, K. Nones, P. Cowin, K. Alsop, Peter Bailey and 71 more. Nature, 2015

1,504 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Reproductive Medicine

View Paper: https://www.semanticscholar.org/paper/b0ef7f2c8324c437866ccc57e60f4f283f210c5a

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Citations in the corpus

HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational-signatures (2017, methodology): “Previously, base-substitution signature 3 was shown to distinguish germline BRCA1 / BRCA2 -null cancers from sporadic cancers in a small subset of breast cancers 29,30 and was subsequently extended to pancreatic 32,33 , ovarian 34 and stomach 35 cancers.”
The Dualistic Model of Ovarian Carcinogenesis: Revisited, Revised, and Expanded. (2016, background): “Recent genome-wide studies have elucidated the mechanisms underlying chemoresistance, and these may potentially lead to new therapeutic strategies that target these pathways.(38,103) It should be noted that these new approaches may improve the progression-free survival, they are less likely to affec”
Genomic Evolution of Breast Cancer Metastasis and Relapse (2017, background): “This is reminiscent of the frequency of parallel evolution of resistance to PARP inhibitors in ovarian cancers through BRCA1/2 reversion mutations (Patch et al., 2015).”
Genomic Hallmarks and Structural Variation in Metastatic Prostate Cancer. (2018, positive): “Our data emphasize that structural variations may inactivate tumor suppressors by disrupting the coding region of these genes (Patch et al., 2015; Waddell et al., 2015), whereas both fusions and alterations affecting intergenic regulatory elements appear to activate driver genes.”
Homologous recombination deficiency: Exploiting the fundamental vulnerability of ovarian cancer (2015, background): “Extensive tumor desmoplasia has also been suggested as a mechanism of resistance in a BRCA1-mutated tumor without BRCA1 reversion (145).”
ESMO–ESGO consensus conference recommendations on ovarian cancer: pathology and molecular biology, early and advanced stages, borderline tumours and recurrent disease (2019, background): “the role of non-HRD molecular mechanisms in resistance development.(51) 52 An association between excision repair cross-complementation group 1 (ERCC1) polymorphism and platinum sensitivity”
Genomic analyses identify molecular subtypes of pancreatic cancer (2016, neutral): “MLL2 (20) PPP6R3 (9) Coverage = 23% (105/456 samples)”