NIH R01 · 2024
PROJECT SUMMARY Homologous recombination (HR), a pathway that repairs DNA double strand breaks (DSB), is frequently mutated in cancers. HR-deficient cancers are prone to genomic instability and are critically dependent on other DNA repair mechanisms for survival. Among them is the DNA damage sensor PARP, and PARP inhibitors have therefore proved an efficient therapy to eliminate HR-deficient cancers. However, some HR-deficient tumors do not respond to PARP inhibitors, and most tumors eventually relapse and become resistant to the drug. New therapeutic strategies are therefore urgently needed to treat HR-deficient cancers and overcome PARP inhibitor resistance. Among the potential…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.