Poly Tar

Downloa cer chemotherapy exploits limitations in repairing DNA damage in order to kill proliferating nant cells. Recent evidence suggests that cancers within and across tissue types have specific defects A repair pathways, and that these defects may predispose for sensitivity and resistance to various s of cytotoxic agents. Poly (ADP-ribose) polymerase (PARP) and BRCA proteins are central to the of DNA strand breaks and, when defective, lead to the accumulation of mutations introduced by rone DNA repair. Breast, ovarian, and other cancers develop in the setting of BRCA deficiency, and cancers may be more sensitive to cytotoxic agents that induce DNA strand breaks, as well as inhiof PARP activity. A series of recent clinical trials has tested whether PARP inhibitors can achieve etic lethality in BRCA-pathway-deficient tumors. Future studies must seek to identify sporadic synth cancers that harbor genomic instability, rendering susceptibility to agents that induce additional and lethal DNA damage. Clin Cancer Res; 16(18); 4517–26. ©2010 AACR.