Abstract
The discovery that homologous recombination deficiency (HRD), a DNA repair defect present in tumours with BRCA1 or BRCA2 (BRCA1/2) mutations, can prevent affected cells from overcoming replicative or drug-induced DNA double-strand breaks both suggested a new therapeutic possibility and explained the observed heterogeneity of chemotherapy effectiveness in women with ovarian cancer. Oral PARP inhibitors were predictably active against BRCA1/2-mutated tumours, by disrupting other DNA repair mechanisms,1 an effect known as synthetic lethality.
Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
