 Cancer cells with BRCA mutations have deficiencies in homologous recombination , and drugs to exploit those deficiencies have been developed and used successfully in clinical trials . Olaparib , a PARP1 inhibitor , shrunk or stopped the growth of tumors from breast , ovarian and prostate cancers caused by mutations in the BRCA1 or BRCA2 genes , which are necessary for HR . When BRCA1 or BRCA2 is absent , other types of DNA repair mechanisms must compensate for the deficiency of HR , such as base @-@ excision repair ( BER ) for stalled replication forks or non @-@ homologous end joining ( NHEJ ) for double strand breaks . By inhibiting BER in an HR @-@ deficient cell , olaparib applies the concept of synthetic lethality to specifically target cancer cells . While PARP1 inhibitors represent a novel approach to cancer therapy , researchers have cautioned that they may prove insufficient for treating late @-@ stage metastatic cancers . Cancer cells can become resistant to a PARP1 inhibitor if they undergo deletions of mutations in BRCA2 , undermining the drug 's synthetic lethality by restoring cancer cells ' ability to repair DNA by HR . 
