Abstract
Defects in homologous recombination (HR) pathway members play a major role in tumorigenesis and predisposition to cancer. HR deficiency (HRD) confers cellular susceptibility to agents that promote cytotoxic double-strand breaks (DSBs); this principle has led to the development and approval of poly (ADP ribose) polymerase (PARP) inhibitors for use in BRCA-mutant breast and ovarian cancers. PARP inhibitors are currently subject to >100 ongoing clinical trials in a wide spectrum of cancer types. Although these approvals have injected new excitement into the field, many challenges remain in detection and interpretation of clinically relevant variants in BRCA1/2 and other genes in the HR pathway.
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