RAD51 and PALB2 in precision oncology: Clinical implications for HRD associated breast and ovarian cancers (Review).

Abstract

Maintaining genomic stability is essential for reducing the risk of carcinogenesis. Homologous recombination (HR) is a high‑fidelity DNA repair mechanism that addresses double‑strand breaks and interstrand crosslinks. The present review examined two key components of HR: RAD51, the eukaryotic recombinase and PALB2, a scaffolding protein. Their structural and functional roles are explored in the context of breast and ovarian cancer. RAD51 facilitates homology search and strand invasion, while PALB2 links BRCA1 and BRCA2, stabilizing RAD51 filaments. Mutations in these genes compromise HR, increasing susceptibility to various cancers and impacting treatment efficacy by impairing DNA repair. The present review discussed the clinical implications of RAD51 and PALB2 mutations, focusing on risk stratification, PARP inhibitor efficacy and emerging therapies. Additionally, it highlighted the potential of RAD51 and PALB2 as biomarkers and therapeutic targets, contributing to advances in personalized cancer management.