The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability

The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability

Cancer is a disease associated with genomic instability and mutations. Excluding some tumors with specific chromosomal translocations, most cancers that develop at an advanced age are characterized by either chromosomal or microsatellite instability. However, it is still unclear how genomic instabil...

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Main Authors: Mitsuko Masutani, Hirobumi Teraoka, Yuko Atsumi, Hirokazu Fukuda, Ken-ichi Yoshioka
Format: Article
Language:English
Published: MDPI AG 2012-05-01
Series:International Journal of Molecular Sciences
Subjects:
cancer
immortality
senescence
genome stability
tetraploidy
H2AX
Arf/p53
Online Access:http://www.mdpi.com/1422-0067/13/5/6492
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spelling doaj-39a7bebc8ffe485e87ea5867b01e8f212020-11-25T01:59:16ZengMDPI AGInternational Journal of Molecular Sciences1422-00672012-05-011356492650610.3390/ijms13056492The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome StabilityMitsuko MasutaniHirobumi TeraokaYuko AtsumiHirokazu FukudaKen-ichi YoshiokaCancer is a disease associated with genomic instability and mutations. Excluding some tumors with specific chromosomal translocations, most cancers that develop at an advanced age are characterized by either chromosomal or microsatellite instability. However, it is still unclear how genomic instability and mutations are generated during the process of cellular transformation and how the development of genomic instability contributes to cellular transformation. Recent studies of cellular regulation and tetraploidy development have provided insights into the factors triggering cellular transformation and the regulatory mechanisms that protect chromosomes from genomic instability.http://www.mdpi.com/1422-0067/13/5/6492cancerimmortalitysenescencegenome stabilitytetraploidyH2AXArf/p53
collection DOAJ
language English
format Article
sources DOAJ
author Mitsuko Masutani
Hirobumi Teraoka
Yuko Atsumi
Hirokazu Fukuda
Ken-ichi Yoshioka
spellingShingle Mitsuko Masutani
Hirobumi Teraoka
Yuko Atsumi
Hirokazu Fukuda
Ken-ichi Yoshioka
The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
International Journal of Molecular Sciences
cancer
immortality
senescence
genome stability
tetraploidy
H2AX
Arf/p53
author_facet Mitsuko Masutani
Hirobumi Teraoka
Yuko Atsumi
Hirokazu Fukuda
Ken-ichi Yoshioka
author_sort Mitsuko Masutani
title The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
title_short The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
title_full The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
title_fullStr The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
title_full_unstemmed The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability
title_sort quiescent cellular state is arf/p53-dependent and associated with h2ax downregulation and genome stability
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2012-05-01
description Cancer is a disease associated with genomic instability and mutations. Excluding some tumors with specific chromosomal translocations, most cancers that develop at an advanced age are characterized by either chromosomal or microsatellite instability. However, it is still unclear how genomic instability and mutations are generated during the process of cellular transformation and how the development of genomic instability contributes to cellular transformation. Recent studies of cellular regulation and tetraploidy development have provided insights into the factors triggering cellular transformation and the regulatory mechanisms that protect chromosomes from genomic instability.
topic cancer
immortality
senescence
genome stability
tetraploidy
H2AX
Arf/p53
url http://www.mdpi.com/1422-0067/13/5/6492
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