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Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer

The cell cycle is the cascade of events that allows a growing cell to duplicate all its components and split into two daughter cells. Cell cycle progression is mediated by the activation of a highly conserved family of protein kinases, the cyclin-dependent kinases (CDKs). CDKs are also regulated by...

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Autores principales: Baldi, Alfonso, De Luca, Antonio, Esposito, Vincenzo, Campioni, Mara, Spugnini, Enrico P., Citro, Gennaro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189597/
https://www.ncbi.nlm.nih.gov/pubmed/22007345
http://dx.doi.org/10.4061/2011/605042
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author Baldi, Alfonso
De Luca, Antonio
Esposito, Vincenzo
Campioni, Mara
Spugnini, Enrico P.
Citro, Gennaro
author_facet Baldi, Alfonso
De Luca, Antonio
Esposito, Vincenzo
Campioni, Mara
Spugnini, Enrico P.
Citro, Gennaro
author_sort Baldi, Alfonso
collection PubMed
description The cell cycle is the cascade of events that allows a growing cell to duplicate all its components and split into two daughter cells. Cell cycle progression is mediated by the activation of a highly conserved family of protein kinases, the cyclin-dependent kinases (CDKs). CDKs are also regulated by related proteins called cdk inhibitors grouped into two families: the INK4 inhibitors (p16, p15, p19, and p18) and the Cip/Kip inhibitors (p21, p27, and p53). Several studies report the importance of cell-cycle proteins in the pathogenesis and the prognosis of lung cancer. This paper will review the most recent data from the literature about the regulation of cell cycle. Finally, based essentially on the data generated in our laboratory, the expression, the diagnostic, and prognostic significance of cell-cycle molecules in lung cancer will be examined.
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spelling pubmed-31895972011-10-17 Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer Baldi, Alfonso De Luca, Antonio Esposito, Vincenzo Campioni, Mara Spugnini, Enrico P. Citro, Gennaro Patholog Res Int Review Article The cell cycle is the cascade of events that allows a growing cell to duplicate all its components and split into two daughter cells. Cell cycle progression is mediated by the activation of a highly conserved family of protein kinases, the cyclin-dependent kinases (CDKs). CDKs are also regulated by related proteins called cdk inhibitors grouped into two families: the INK4 inhibitors (p16, p15, p19, and p18) and the Cip/Kip inhibitors (p21, p27, and p53). Several studies report the importance of cell-cycle proteins in the pathogenesis and the prognosis of lung cancer. This paper will review the most recent data from the literature about the regulation of cell cycle. Finally, based essentially on the data generated in our laboratory, the expression, the diagnostic, and prognostic significance of cell-cycle molecules in lung cancer will be examined. SAGE-Hindawi Access to Research 2011 2011-10-05 /pmc/articles/PMC3189597/ /pubmed/22007345 http://dx.doi.org/10.4061/2011/605042 Text en Copyright © 2011 Alfonso Baldi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Baldi, Alfonso
De Luca, Antonio
Esposito, Vincenzo
Campioni, Mara
Spugnini, Enrico P.
Citro, Gennaro
Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title_full Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title_fullStr Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title_full_unstemmed Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title_short Tumor Suppressors and Cell-Cycle Proteins in Lung Cancer
title_sort tumor suppressors and cell-cycle proteins in lung cancer
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189597/
https://www.ncbi.nlm.nih.gov/pubmed/22007345
http://dx.doi.org/10.4061/2011/605042
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