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Updated: Nov 29, 2025

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Genomic destabilization and its associated mutagenesis increase with senescence-associated phenotype expression
Ken-Ichi Yoshioka1, Yusuke Matsuno1,2
1Laboratory of Genome Stability Maintenance, National Cancer Center Research Institute, Tokyo, Japan.
Abstract:
Cancer develops through multiple rounds of clonal evolution of cells with abrogated defense systems. Such clonal evolution is triggered by genomic destabilization with associated mutagenesis. However, what increases the risk of genomic destabilization remains unclear. Genomic instability is usually the result of erroneous repair of DNA double-strand breaks (DSB); paradoxically, however, most cancers develop with genomic instability but lack mutations in DNA repair systems. In this manuscript, we review current knowledge regarding a cellular state that increases the risk of genomic destabilization, in which cells exhibit phenotypes often observed during senescence. In addition, we explore the pathways that lead to genomic destabilization and its associated mutagenesis, which ultimately result in cancer.
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