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Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies
Conventional chemotherapeutics target the proliferating fraction of cells in the patient’s body, which will include the tumor cells, but are also toxic to actively proliferating normal tissues. Cellular stresses, such as those imposed by chemotherapeutic drugs, induce cell cycle checkpoint arrest, a...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Research Foundation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270485/ https://www.ncbi.nlm.nih.gov/pubmed/22347187 http://dx.doi.org/10.3389/fphar.2012.00009 |
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author | Gabrielli, Brian Brooks, Kelly Pavey, Sandra |
author_facet | Gabrielli, Brian Brooks, Kelly Pavey, Sandra |
author_sort | Gabrielli, Brian |
collection | PubMed |
description | Conventional chemotherapeutics target the proliferating fraction of cells in the patient’s body, which will include the tumor cells, but are also toxic to actively proliferating normal tissues. Cellular stresses, such as those imposed by chemotherapeutic drugs, induce cell cycle checkpoint arrest, and currently approaches targeting these checkpoints are being explored to increase the efficacy and selectivity of conventional chemotherapeutic treatments. Loss of a checkpoint may also make cancer cells more reliant on other mechanisms to compensate for the loss of this function, and these compensatory mechanisms may be targeted using synthetic lethal approaches. Here we will discuss the utility of targeting checkpoint defects as novel anti-cancer therapies. |
format | Online Article Text |
id | pubmed-3270485 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Frontiers Research Foundation |
record_format | MEDLINE/PubMed |
spelling | pubmed-32704852012-02-15 Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies Gabrielli, Brian Brooks, Kelly Pavey, Sandra Front Pharmacol Pharmacology Conventional chemotherapeutics target the proliferating fraction of cells in the patient’s body, which will include the tumor cells, but are also toxic to actively proliferating normal tissues. Cellular stresses, such as those imposed by chemotherapeutic drugs, induce cell cycle checkpoint arrest, and currently approaches targeting these checkpoints are being explored to increase the efficacy and selectivity of conventional chemotherapeutic treatments. Loss of a checkpoint may also make cancer cells more reliant on other mechanisms to compensate for the loss of this function, and these compensatory mechanisms may be targeted using synthetic lethal approaches. Here we will discuss the utility of targeting checkpoint defects as novel anti-cancer therapies. Frontiers Research Foundation 2012-02-02 /pmc/articles/PMC3270485/ /pubmed/22347187 http://dx.doi.org/10.3389/fphar.2012.00009 Text en Copyright © 2012 Gabrielli, Brooks and Pavey. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
spellingShingle | Pharmacology Gabrielli, Brian Brooks, Kelly Pavey, Sandra Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title | Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title_full | Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title_fullStr | Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title_full_unstemmed | Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title_short | Defective Cell Cycle Checkpoints as Targets for Anti-Cancer Therapies |
title_sort | defective cell cycle checkpoints as targets for anti-cancer therapies |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270485/ https://www.ncbi.nlm.nih.gov/pubmed/22347187 http://dx.doi.org/10.3389/fphar.2012.00009 |
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