@misc{oai:repo.qst.go.jp:00070272,
 author = {Yamauchi, Masatake and Fukutsu, Kumiko and Sakagami, Mari and Yamada, Yuji and 山内 正剛 and 福津 久美子 and 坂上 万里 and 山田 裕司},
 month = {Sep},
 note = {To investigate the initial processes involved in radiation carcinogenesis, we isolated and examined mouse mutant cells exhibiting phenotype plasticity.  Approximately 10% of 6-thioguanine resistant (6TGR) cells derived from the irradiated cell population exhibited phenotype plasticity and reverted to wild type HAT resistance (HATR).  Similar mutant cells were also identified in an un-irradiated wild type cell population, but at a lower frequency.  Ionizing irradiation enhanced the frequency of the plastic mutation approximately 24 times in our experiment.  Treatment with 5-aza-cytidine did not affect phenotype plasticity.  Detailed molecular analysis of the promoter region of the hypoxanthine phosphoribosyl transferase (Hprt) gene revealed that most cytidine residues were not methylated, even in 6TGR mutant cells, in which Hprt activity must be down-regulated.  These results suggested that DNA methylation was not involved in mutant phenotype plasticity.  We have identified a new type of genomic instability induced by ionizing radiation.  Plasticity in gene regulation may play an important role in radiation carcinogenesis, which is a multiple-stages process., 欧州エピジェネティクス会議},
 title = {Identification of mouse mutant cells exhibiting the plastic mutant phenotype},
 year = {2010}
}