PARP Inhibitors in Cancer Therapy: Promise, Progress, and Puzzles Leif W. Ellisen  Cancer Cell  Volume 19, Issue 2, Pages 165-167 (February 2011) DOI: 10.1016/j.ccr.2011.01.047 Copyright © 2011 Elsevier Inc. Terms and Conditions

Figure 1 PARP Inhibitor Treatment of BRCA1/2-Associated and Sporadic Cancers Normal cells have intact base excision repair and homologous recombination that are mediated by PARP and BRCA1/2-dependent pathways, respectively. In germline BRCA1 or BRCA2 mutation carriers, the capacity for HR is often lost during tumorigenesis due to the inactivation of the remaining wild-type allele. PARP inhibitor treatment disables the repair of spontaneous DNA damage in these tumor cells, leading to their death. Sporadic tumors including triple-negative breast cancer may have defects in BRCA1/2 expression and/or function. Treatment combining a PARP inhibitor with DNA-damaging chemotherapy may be an effective strategy for some of these tumors. (Illustration courtesy of Zachary Nash.) Cancer Cell 2011 19, 165-167DOI: (10.1016/j.ccr.2011.01.047) Copyright © 2011 Elsevier Inc. Terms and Conditions