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How does tumor suppressor FHIT modulate oxidative stress and DNA damage checkpoints in early cancer?
https://repo.qst.go.jp/records/45633
https://repo.qst.go.jp/records/456335d122660-61f4-4b11-ab67-975c225f32e8
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2009-09-14 | |||||
| タイトル | ||||||
| タイトル | How does tumor suppressor FHIT modulate oxidative stress and DNA damage checkpoints in early cancer? | |||||
| 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 | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Ishii, Hideshi
× Ishii, Hideshi× Saito, Toshiyuki× 齋藤 俊行 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Oxidative stress, a biochemical condition that is characterized by an imbalance between the presence of relatively high levels of toxic reactive species and antioxidative defense mechanisms, has been linked to various cellular philology and disorders characterized by cell death, such as stem cells of neural and hematopoietic systems. Recent studies indicate that common chromosome fragile sites, non-random targets of double stranded breaks under replication perturbation that are characteristic of tumors, paradoxically encode the tumor suppressor FHIT gene, which modulates response to oxidative stress and DNA damage. Since it is inactivated in precancer or early stages of carcinogenesis, we propose that the FHIT gene plays a role in the creation of cancer initiating cells. Mechanistic roles of FHIT in modulating oxidative stress and DNA damage checkpoints of cancer initiating cells are also discussed. | |||||
| 書誌情報 |
Progress in DNA Damage Research (Nova Biomedical) p. 243-251, 発行日 2008-07 |
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| 出版者 | ||||||
| 出版者 | Nova Science Publishers | |||||
| ISBN | ||||||
| 識別子タイプ | ISBN | |||||
| 関連識別子 | 978-1-6045-6582 | |||||
