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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...

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Detalles Bibliográficos
Autores principales: Gabrielli, Brian, Brooks, Kelly, Pavey, Sandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
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.
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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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