Capitalizing on Cancer Replication Stress by Preventing PAR Chain Turnover: A New Type of Synthetic Lethality.
| Autor: | McDermott N; Molecular Biology Program and Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA., Buechelmaier ES; Molecular Biology Program and Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Weill Cornell Medicine, Graduate School of Medical Sciences, New York, NY 10065, USA., Powell SN; Molecular Biology Program and Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: powells@mskcc.org. |
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| Jazyk: | angličtina |
| Zdroj: | Cancer cell [Cancer Cell] 2019 Mar 18; Vol. 35 (3), pp. 344-346. |
| DOI: | 10.1016/j.ccell.2019.02.011 |
| Abstrakt: | Tumors resistant to PARP inhibitors frequently show signs of replication stress, with hyper-activated PARP. In this issue of Cancer Cell, Pillay et al. demonstrate that inhibiting PAR-chain turnover results in cell-cycle arrest, which is cytotoxic when combined with cell-cycle checkpoint inhibition and constitutes a novel cancer therapy. (Copyright © 2019 Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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