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Updated: May 20, 2026

Quantification of γH2AX Foci in Response to Ionising Radiation
Published on: April 6, 2010
The quiescent cellular state is Arf/p53-dependent and associated with H2AX downregulation and genome stability
Ken-Ichi Yoshioka1, Yuko Atsumi1,2, Hirokazu Fukuda3
1Division of Genome Stability Research, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
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.
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