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Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer
Aberrant gene silencing is highly associated with altered cell cycle regulation during carcinogenesis. In particular, silencing of the CDKN2A tumor suppressor gene, which encodes the p16(INK4a) protein, has a causal link with several different types of cancers. The p16(INK4a) protein plays an execut...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919535/ https://www.ncbi.nlm.nih.gov/pubmed/27428416 http://dx.doi.org/10.1016/j.ebiom.2016.04.017 |
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author | Zhao, Ran Choi, Bu Young Lee, Mee-Hyun Bode, Ann M. Dong, Zigang |
author_facet | Zhao, Ran Choi, Bu Young Lee, Mee-Hyun Bode, Ann M. Dong, Zigang |
author_sort | Zhao, Ran |
collection | PubMed |
description | Aberrant gene silencing is highly associated with altered cell cycle regulation during carcinogenesis. In particular, silencing of the CDKN2A tumor suppressor gene, which encodes the p16(INK4a) protein, has a causal link with several different types of cancers. The p16(INK4a) protein plays an executional role in cell cycle and senescence through the regulation of the cyclin-dependent kinase (CDK) 4/6 and cyclin D complexes. Several genetic and epigenetic aberrations of CDKN2A lead to enhanced tumorigenesis and metastasis with recurrence of cancer and poor prognosis. In these cases, the restoration of genetic and epigenetic reactivation of CDKN2A is a practical approach for the prevention and therapy of cancer. This review highlights the genetic status of CDKN2A as a prognostic and predictive biomarker in various cancers. |
format | Online Article Text |
id | pubmed-4919535 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-49195352016-06-30 Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer Zhao, Ran Choi, Bu Young Lee, Mee-Hyun Bode, Ann M. Dong, Zigang EBioMedicine Review Aberrant gene silencing is highly associated with altered cell cycle regulation during carcinogenesis. In particular, silencing of the CDKN2A tumor suppressor gene, which encodes the p16(INK4a) protein, has a causal link with several different types of cancers. The p16(INK4a) protein plays an executional role in cell cycle and senescence through the regulation of the cyclin-dependent kinase (CDK) 4/6 and cyclin D complexes. Several genetic and epigenetic aberrations of CDKN2A lead to enhanced tumorigenesis and metastasis with recurrence of cancer and poor prognosis. In these cases, the restoration of genetic and epigenetic reactivation of CDKN2A is a practical approach for the prevention and therapy of cancer. This review highlights the genetic status of CDKN2A as a prognostic and predictive biomarker in various cancers. Elsevier 2016-05-03 /pmc/articles/PMC4919535/ /pubmed/27428416 http://dx.doi.org/10.1016/j.ebiom.2016.04.017 Text en © 2016 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Review Zhao, Ran Choi, Bu Young Lee, Mee-Hyun Bode, Ann M. Dong, Zigang Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title | Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title_full | Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title_fullStr | Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title_full_unstemmed | Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title_short | Implications of Genetic and Epigenetic Alterations of CDKN2A (p16(INK4a)) in Cancer |
title_sort | implications of genetic and epigenetic alterations of cdkn2a (p16(ink4a)) in cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919535/ https://www.ncbi.nlm.nih.gov/pubmed/27428416 http://dx.doi.org/10.1016/j.ebiom.2016.04.017 |
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