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Moving beyond PARP Inhibition in ATM-Deficient Prostate Cancer
DNA repair defects are found in primary and metastatic prostate cancer. Alterations in the ATM gene are the second most common defect after BRCA2, but their sensitivity to PARP inhibitors has been questioned by recent clinical literature. The work by Rafiei and colleagues in this issue of Cancer Res...
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Published in: | Cancer research (Chicago, Ill.) Ill.), 2020-06, Vol.80 (11), p.2085-2086 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | DNA repair defects are found in primary and metastatic prostate cancer. Alterations in the ATM gene are the second most common defect after BRCA2, but their sensitivity to PARP inhibitors has been questioned by recent clinical literature. The work by Rafiei and colleagues in this issue of Cancer Research 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.
See related article by Rafiei et al., p. 2094 |
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ISSN: | 0008-5472 1538-7445 |
DOI: | 10.1158/0008-5472.CAN-20-0966 |