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The inability to repair double stranded DNA breaks, or homologous recombination deficiency (HRD), is the first clinically actionable molecular aberration to be identified in gynecologic cancers. Germline mutations in BRCA1 and BRCA2 were the first biomarkers of this phenotype to be identified. Further investigation of these mutations revealed that they are key biomarkers for prevention in affected blood relatives, improved prognosis, response to platinum-based therapy, and, of more recent importance, maximum benefit from poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor (PARPi) treatment [1]. Mutations in additional genes including RAD51C, RAD51D, BRIP1, ATM, CHEK2, BARD1, MRE11, NBS1, PALB2, and NBN are now also implicated in this pathway and are rationale predictors of PARPi sensitivity [2-4], as loss of their protein products impair the homologous recombination (HR) pathway's task to maintain genomic stability [5]. The Cancer Genome Atlas (TCGA) project in the USA reported up to alterations in the HR pathway in 51% of high grade serous ovarian cancers, with 16% of tumors harboring germline BRCA1 or BRCA2 mutations, 9% with somatic mutations, and 11% with epigenetic silencing of BRCA1 by way of methylation [6].

Role and clinical application of next-generation sequencing (NGS) for ovarian cancer