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Targeting the Checkpoint to Kill Cancer Cells
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 damag...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598780/ https://www.ncbi.nlm.nih.gov/pubmed/26295265 http://dx.doi.org/10.3390/biom5031912 |
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author | Benada, Jan Macurek, Libor |
author_facet | Benada, Jan Macurek, Libor |
author_sort | Benada, Jan |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4598780 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-45987802015-10-15 Targeting the Checkpoint to Kill Cancer Cells Benada, Jan Macurek, Libor Biomolecules Review 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. MDPI 2015-08-18 /pmc/articles/PMC4598780/ /pubmed/26295265 http://dx.doi.org/10.3390/biom5031912 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Benada, Jan Macurek, Libor Targeting the Checkpoint to Kill Cancer Cells |
title | Targeting the Checkpoint to Kill Cancer Cells |
title_full | Targeting the Checkpoint to Kill Cancer Cells |
title_fullStr | Targeting the Checkpoint to Kill Cancer Cells |
title_full_unstemmed | Targeting the Checkpoint to Kill Cancer Cells |
title_short | Targeting the Checkpoint to Kill Cancer Cells |
title_sort | targeting the checkpoint to kill cancer cells |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598780/ https://www.ncbi.nlm.nih.gov/pubmed/26295265 http://dx.doi.org/10.3390/biom5031912 |
work_keys_str_mv | AT benadajan targetingthecheckpointtokillcancercells AT macureklibor targetingthecheckpointtokillcancercells |