Moving beyond PARP Inhibition in ATM-Deficient Prostate Cancer.

DNA repair defects are found in primary and metastatic prostate cancer. Alterations in the gene are the second most common defect after , but their sensitivity to PARP inhibitors has been questioned by recent clinical literature. The work by Rafiei and colleagues in this issue of now supports this observation with genetically engineered cells and quantitative responses. ATR inhibitors have not yet found a clear role in the clinic, but the new work suggests that ATM-deficient cancers may be more vulnerable to ATR inhibition rather than PARP inhibitors, which is a testable hypothesis for clinical trials..