Abstract
Objective: 53BP1 is a critical regulator of the balance between homologous recombination (HR) and the more error-prone nonhomologous endjoining (NHEJ) DNA repair. Deletion of 53BP1 in brca1- (but not brca2-) null cells rescues embryonic lethality, partially restores HR, and reverses sensitivity to poly-ADP ribose polymerase inhibitors (PARPi). We characterized 53BP1 and BRCA1 expression in a large number of primary and recurrent ovarian carcinomas to determine if 53BP1 expression is associated with clinical outcomes in sporadic and inherited cases.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
