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Calorie restriction alters the mechanisms of radiation-induced mouse thymic lymphomagenesis
http://hdl.handle.net/10069/00042045
http://hdl.handle.net/10069/000420452faffde6-2ce9-4a67-b42d-7271f5a13c0d
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2023-02-10 | |||||
タイトル | ||||||
タイトル | Calorie restriction alters the mechanisms of radiation-induced mouse thymic lymphomagenesis | |||||
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 |
Nakayama, Takafumi
× Nakayama, Takafumi× Sunaoshi, Masaaki× Shang, Yi× Takahashi, Mizuki× Saito, Takato× Blyth, Benjamin J.× Amasaki, Yoshiko× Daino, Kazuhiro× Shimada, Yoshiya× Tachibana, Akira× Kakinuma, Shizuko |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Calorie restriction (CR) suppresses not only spontaneous but also chemical- and radiation-induced carcinogenesis. Our previous study revealed that the cancer-preventive effect of CR is tissue dependent and that CR does not effectively prevent the development of thymic lymphoma (TL). We investigated the association between CR and the genomic alterations of resulting TLs to clarify the underlying resistance mechanism. TLs were obtained from previous and new experiments, in which B6C3F1 mice were exposed to radiation at 1 week of age and fed with a CR or standard (non-CR) diet from 7 weeks throughout their lifetimes. All available TLs were used for analysis of genomic DNA. In contrast to the TLs of the non-CR group, those of the CR group displayed suppression of copy-neutral loss of heterozygosity (LOH) involving relevant tumor suppressor genes (Cdkn2a, Ikzf1, Trp53, Pten), an event regarded as cell division–associated. However, CR did not affect interstitial deletions of those genes, which were observed in both groups. In addition, CR affected the mechanism of Ikzf1 inactivation in TLs: the non-CR group exhibited copy-neutral LOH with duplicated inactive alleles, whereas the CR group showed expression of dominant-negative isoforms accompanying a point mutation or an intragenic deletion. These results suggest that, even though CR reduces cell division–related genomic rearrangements by suppressing cell proliferation, tumors arise via diverse carcinogenic pathways including inactivation of tumor suppressors via interstitial deletions and other mutations. These findings provide a molecular basis for improved prevention strategies that overcome the CR resistance of lymphomagenesis. | |||||
書誌情報 |
PLOS ONE 巻 18, 号 1, p. e0280560, 発行日 2023-01-20 |
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出版者 | ||||||
出版者 | PLOS | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1932-6203 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1371/journal.pone.0280560 | |||||
権利 | ||||||
権利情報 | © 2023 Nakayama 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, 18(1), art. no. e0280560; 2023 |