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Int. J. Mol. Sci. 2012, 13(5), 6492-6506; doi:10.3390/ijms13056492

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

1
Division of Genome Stability Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
2
Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara 228-8555, Japan
3
Division of Cancer Development System, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
4
Department of Pathological Biochemistry, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan
*
Author to whom correspondence should be addressed.
Received: 11 April 2012 / Revised: 21 May 2012 / Accepted: 22 May 2012 / Published: 24 May 2012
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Abstract

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. View Full-Text
Keywords: cancer; immortality; senescence; genome stability; tetraploidy; H2AX; Arf/p53 cancer; immortality; senescence; genome stability; tetraploidy; H2AX; Arf/p53
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This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Yoshioka, K.-I.; Atsumi, Y.; Fukuda, H.; Masutani, M.; Teraoka, H. The Quiescent Cellular State is Arf/p53-Dependent and Associated with H2AX Downregulation and Genome Stability. Int. J. Mol. Sci. 2012, 13, 6492-6506.

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