Abstract
RAD51C and RAD51D are two paralogs of RAD51, essential for the repair of DNA breaks by homologous recombination (HRR). Germline pathogenic variants (PV) in these genes have been associated with HRR deficiency (HRD) and antitumor response to DNA damaging agents, including PARP inhibitors. The evaluation of RAD51 nuclear foci provides a functional measure of HRD, whereas genomic HRD captures accumulated tumor genomic instability. Biallelic inactivation of RAD51C has been associated with genomic HRD.
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