Clinical anticancer drug development: targeting the cyclin-dependent kinases

Cell division involves a cyclical biochemical process composed of several step-wise reactions that have to occur once per cell cycle. Dysregulation of cell division is a hallmark of all cancers. Genetic and epigenetic mechanisms frequently result in deranged expression and/or activity of cell-cycle...

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Detalles Bibliográficos
Autores principales: Benson, C, Kaye, S, Workman, P, Garrett, M, Walton, M, de Bono, J
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2005
Materias:
Minireview
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361734/
https://www.ncbi.nlm.nih.gov/pubmed/15558073
http://dx.doi.org/10.1038/sj.bjc.6602229
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author Benson, C
Kaye, S
Workman, P
Garrett, M
Walton, M
de Bono, J
author_facet Benson, C
Kaye, S
Workman, P
Garrett, M
Walton, M
de Bono, J
author_sort Benson, C
collection PubMed
description Cell division involves a cyclical biochemical process composed of several step-wise reactions that have to occur once per cell cycle. Dysregulation of cell division is a hallmark of all cancers. Genetic and epigenetic mechanisms frequently result in deranged expression and/or activity of cell-cycle proteins including the cyclins, cyclin-dependent kinases (Cdks), Cdk inhibitors and checkpoint control proteins. The critical nature of these proteins in cell cycling raises hope that targeting them may result in selective cytotoxicity and valuable anticancer activity.
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spelling pubmed-23617342009-09-10 Clinical anticancer drug development: targeting the cyclin-dependent kinases Benson, C Kaye, S Workman, P Garrett, M Walton, M de Bono, J Br J Cancer Minireview Cell division involves a cyclical biochemical process composed of several step-wise reactions that have to occur once per cell cycle. Dysregulation of cell division is a hallmark of all cancers. Genetic and epigenetic mechanisms frequently result in deranged expression and/or activity of cell-cycle proteins including the cyclins, cyclin-dependent kinases (Cdks), Cdk inhibitors and checkpoint control proteins. The critical nature of these proteins in cell cycling raises hope that targeting them may result in selective cytotoxicity and valuable anticancer activity. Nature Publishing Group 2005-01-17 2004-11-23 /pmc/articles/PMC2361734/ /pubmed/15558073 http://dx.doi.org/10.1038/sj.bjc.6602229 Text en Copyright © 2005 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Minireview
Benson, C
Kaye, S
Workman, P
Garrett, M
Walton, M
de Bono, J
Clinical anticancer drug development: targeting the cyclin-dependent kinases
title Clinical anticancer drug development: targeting the cyclin-dependent kinases
title_full Clinical anticancer drug development: targeting the cyclin-dependent kinases
title_fullStr Clinical anticancer drug development: targeting the cyclin-dependent kinases
title_full_unstemmed Clinical anticancer drug development: targeting the cyclin-dependent kinases
title_short Clinical anticancer drug development: targeting the cyclin-dependent kinases
title_sort clinical anticancer drug development: targeting the cyclin-dependent kinases
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361734/
https://www.ncbi.nlm.nih.gov/pubmed/15558073
http://dx.doi.org/10.1038/sj.bjc.6602229
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AT waltonm clinicalanticancerdrugdevelopmenttargetingthecyclindependentkinases
AT debonoj clinicalanticancerdrugdevelopmenttargetingthecyclindependentkinases

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