Capitalizing on cancer replication stress by preventing PAR chain turnover: A new type of synthetic lethality Editorial


Authors: McDermott, N.; Buechelmaier, E. S.; Powell, S. N.
Title: Capitalizing on cancer replication stress by preventing PAR chain turnover: A new type of synthetic lethality
Abstract: 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. © 2019 Elsevier Inc.
Keywords: unclassified drug; dna replication; homologous recombination; cell cycle s phase; enzyme inhibition; cytotoxicity; enzyme activity; cell cycle arrest; short survey; cell cycle checkpoint; dna damage response; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase; histone h2ax; single stranded dna break; gamma histone h2ax; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 1; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 2; poly(adenosine diphosphate ribose); g2 phase cell cycle checkpoint; human; priority journal; glycosidase; malignant neoplasm; glycosidase inhibitor; pdd 0001627; poly(adenosine diphosphate ribose)glycosidase
Journal Title: Cancer Cell
Volume: 35
Issue: 3
ISSN: 1535-6108
Publisher: Cell Press  
Date Published: 2019-03-18
Start Page: 344
End Page: 346
Language: English
DOI: 10.1016/j.ccell.2019.02.011
PUBMED: 30889377
PROVIDER: scopus
DOI/URL:
Notes: Source: Scopus
Altmetric
Citation Impact
BMJ Impact Analytics
MSK Authors
  1. Simon Nicholas Powell
    331 Powell