Abstract:Homologous-recombination (HR) deficient tumors with BRCA1 and BRCA2 mutations exhibit replication fork stability defects. To date, PARP inhibitors are the only targeted therapy available in the clinic against HR deficient tumors, and alternative therapies are needed. In this study, we found a deubiquitinase, USP1, to be significantly upregulated in tumors with mutations in BRCA1. SiRNA mediated silencing or small molecule inhibition of USP1 activity resulted in replication fork destabilization and decreased vi… Show more
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