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Targeting the Checkpoint to Kill Cancer Cells

by Jan Benada 1,2 and Libor Macurek 1,*
1
Department of Cancer Cell Biology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, CZ14200 Prague, Czech Republic
2
Department of Genetics and Microbiology, Faculty of Science, Charles University in Prague, CZ12844 Prague, Czech Republic
*
Author to whom correspondence should be addressed.
Academic Editors: Wolf-Dietrich Heyer, Thomas Helleday and Fumio Hanaoka
Biomolecules 2015, 5(3), 1912-1937; https://doi.org/10.3390/biom5031912
Received: 2 July 2015 / Revised: 7 August 2015 / Accepted: 11 August 2015 / Published: 18 August 2015
(This article belongs to the Special Issue DNA Damage Response)
Cancer treatments such as radiotherapy and most of the chemotherapies act by damaging DNA of cancer cells. Upon DNA damage, cells stop proliferation at cell cycle checkpoints, which provides them time for DNA repair. Inhibiting the checkpoint allows entry to mitosis despite the presence of DNA damage and can lead to cell death. Importantly, as cancer cells exhibit increased levels of endogenous DNA damage due to an excessive replication stress, inhibiting the checkpoint kinases alone could act as a directed anti-cancer therapy. Here, we review the current status of inhibitors targeted towards the checkpoint effectors and discuss mechanisms of their actions in killing of cancer cells. View Full-Text
Keywords: checkpoint; DNA damage response; replication stress; cancer; inhibitor; ATM; ATR; Chk1; Wee1; p53 checkpoint; DNA damage response; replication stress; cancer; inhibitor; ATM; ATR; Chk1; Wee1; p53
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Benada, J.; Macurek, L. Targeting the Checkpoint to Kill Cancer Cells. Biomolecules 2015, 5, 1912-1937.

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