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Mouse models of gastric tumors: Wnt activation and PGE<sub>2</sub> induction
https://doi.org/10.24517/00027531
https://doi.org/10.24517/00027531796ae34c-6f7f-4958-ba3c-380daf879f5b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-OSHIMA-M-599.pdf (2.4 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-10-05 | |||||||||
| タイトル | ||||||||||
| タイトル | Mouse models of gastric tumors: Wnt activation and PGE<sub>2</sub> induction | |||||||||
| 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 | |||||||||
| ID登録 | ||||||||||
| ID登録 | 10.24517/00027531 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Oshima, Hiroko
× Oshima, Hiroko× Oshima, Masanobu |
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| 著者別表示 |
大島, 浩子
× 大島, 浩子
× 大島, 正伸
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学がん研究所 | |||||||||
| 書誌情報 |
Pathology International 巻 60, 号 9, p. 599-607, 発行日 2010-09-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 1320-5463 | |||||||||
| NCID | ||||||||||
| 収録物識別子タイプ | NCID | |||||||||
| 収録物識別子 | AA10984364 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isVersionOf | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1111/j.1440-1827.2010.02567.x | |||||||||
| 出版者 | ||||||||||
| 出版者 | Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd / 日本病理学会 | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Accumulating evidence has suggested that cooperation of oncogenic activation and the host responses is important for cancer development. In gastric cancer, activation of Wnt signaling appears to be a major oncogenic pathway that causes tumorigenesis. In the chronic gastritis caused by Helicobacter pylori infection, cyclooxigenase-2 induces prostaglandin E 2 (PGE2) biosythesis, which plays an important role in tumorigenesis. We constructed a series of mouse models and investigated the role of each pathway in the gastric tumorigenesis. Wnt activation in gastric epithelial cells suppresses differentiation, and induces development of preneoplastic lesions. On the other hand, induction of the PGE2 pathway in gastric mucosa induces development of spasmolytic polypeptide-expressing metaplasia (SPEM), which is a possible preneoplastic metaplasia. Importantly, simultaneous activation of Wnt and PGE2 pathways leads to dysplastic gastric tumor development. Moreover, induction of the PGE2 pathway also promotes gastric hamartoma development when bone morphogenetic protein (BMP) signaling is suppressed. These results indicate that alteration in the Wnt or BMP signaling impairs epithelial differentiation, and the PGE2 pathway accelerates tumor formation regardless of the types of oncogenic pathways. We review the phenotypes and gene expression profiles of the respective models, and discuss the cooperation of oncogenic pathways and host responses in gastric tumorigenesis. Copyright © 2010 Japanese Society of Pathology and Blackwell Publishing Asia Pty Ltd. | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
