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Fhit Deficiency-Induced Global Genome Instability Promotes Mutation and Clonal Expansion
http://hdl.handle.net/10069/34280
http://hdl.handle.net/10069/34280942a0891-7832-4e54-be04-3f99f7d0f481
名前 / ファイル | ライセンス | アクション |
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PLoS8_80730.pdf (3.6 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2014-04-17 | |||||
タイトル | ||||||
タイトル | Fhit Deficiency-Induced Global Genome Instability Promotes Mutation and Clonal Expansion | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Miuma, Satoshi
× Miuma, Satoshi× Saldivar, Joshua C.× Karras, Jenna R.× Waters, Catherine E.× Paisie, Carolyn A.× Wang, Yao× Jin, Victor× Sun, Jin× Druck, Teresa× Zhang, Jie× Huebner, Kay |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Loss of Fhit expression, encoded at chromosome fragile site FRA3B, leads to increased replication stress, genome instability and accumulation of genetic alterations. We have proposed that Fhit is a genome 'caretaker' whose loss initiates genome instability in preneoplastic lesions. We have characterized allele copy number alterations and expression changes observed in Fhit-deficient cells in conjunction with alterations in cellular proliferation and exome mutations, using cells from mouse embryo fibroblasts (MEFs), mouse kidney, early and late after establishment in culture, and in response to carcinogen treatment. Fhit-/- MEFs escape senescence to become immortal more rapidly than Fhit+/+ MEFs; -/- MEFs and kidney cultures show allele losses and gains, while +/+ derived cells show few genomic alterations. Striking alterations in expression of p53, p21, Mcl1 and active caspase 3 occurred in mouse kidney -/- cells during progressive tissue culture passage. To define genomic changes associated with preneoplastic changes in vivo, exome DNAs were sequenced for +/+ and -/- liver tissue after treatment of mice with the carcinogen, 7,12-dimethylbenz[a]anthracene, and for +/+ and -/- kidney cells treated in vitro with this carcinogen. The -/- exome DNAs, in comparison with +/+ DNA, showed small insertions, deletions and point mutations in more genes, some likely related to preneoplastic changes. Thus, Fhit loss provides a 'mutator' phenotype, a cellular environment in which mild genome instability permits clonal expansion, through proliferative advantage and escape from apoptosis, in response to pressures to survive. | |||||
書誌情報 |
PLoS ONE 巻 8, 号 11, p. e80730, 発行日 2013-11-14 |
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出版者 | ||||||
出版者 | Public Library of Science | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 19326203 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1371/journal.pone.0080730 | |||||
権利 | ||||||
権利情報 | c 2013 Miuma et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | PLoS ONE, 8(11), e80730; 2013 |