![]() ![]() BRCA1 and RAD51C promoter methylation results in transcriptional silencing 21 and commonly leads to HRD in HGOC 22. However, the extent to which many HRR genes contribute to PARPi sensitivity remains unclear 20. Alterations in other homologous recombination repair (HRR) pathway genes, including PALB2, RAD51C, and RAD51D, have been associated with improved responses to rucaparib and other PARPi 17, 18, 19. ![]() Germline and somatic BRCA1 or BRCA2 ( BRCA) mutations are well-defined biomarkers for PARPi response for a number of cancer types, including breast, ovarian, pancreatic, and prostate 11, 12, 13, 14, 15, 16. Genetic, epigenetic, and genomic biomarkers can suggest the presence of HRD and help identify patients most likely to respond to PARPi 8, 9, 10. Homologous recombination deficiency (HRD) sensitizes neoplasms to rucaparib and other DNA-damaging agents (e.g., platinum-based chemotherapy) 2, 3, and platinum sensitivity in high-grade ovarian carcinoma (HGOC) is a strong clinical predictor of benefit from PARP inhibitors (PARPi) 4, 5, 6, 7. Rucaparib is an inhibitor of poly(ADP-ribose) polymerase (PARP) 1, PARP2, and PARP3, DNA damage repair enzymes in the base excision repair pathway 1. Nature Communications volume 12, Article number: 2487 ( 2021) ![]() Molecular and clinical determinants of response and resistance to rucaparib for recurrent ovarian cancer treatment in ARIEL2 (Parts 1 and 2) ![]()
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