| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○著者 (必須): | 1. | 銭 志栄
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| 2. | (英) Asa L Sylvia (日) (読)
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| 3. | 塩見 春彦
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| 4. | 塩見 美喜子
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| 5. | 吉本 勝彦
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| 6. | (英) Yamada Shozo (日) (読)
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| 7. | (英) Wang Lu Elaine (日) (読)
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| 8. | (英) Rahman Mustafizur Md (日) (読)
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| 9. | 井上 寛
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| 10. | 板倉 光夫
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| 11. | 工藤 英治
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| 12. | 佐野 壽昭
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| ○題名 (必須): | □ | (英) Overexpression of HMGA2 relates to reduction of the let-7 and its relationship to clinicopathological features in pituitary adenomas. (日)
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| ○要約 (任意): | □ | (英) High-mobility group A2 is highly expressed during embryogenesis and in various benign and malignant tumors. Recent studies report that high-mobility group A2 is negatively regulated by the let-7 microRNAs (miRNAs) family in vitro. The development of pituitary adenomas in high-mobility group A2 transgenic mice showed that high-mobility group A2 may be involved in pituitary tumorigenesis. However, no studies have investigated the clinical significance of high-mobility group A2 and its relationship to the let-7 miRNA family in human pituitary adenomas. Using immunohistochemistry, we analyzed high-mobility group A2 expression with respect to various clinicopathologic factors in 98 pituitary adenomas. Overexpression of high-mobility group A2 was observed in 39% (38/98) of pituitary adenomas compared with normal adenohypophysial tissue and was frequently found in adenomas including prolactin (PRL), adrenocorticotrophic hormone, or follicle-stimulating hormone/luteinizing hormone and in null cell adenomas, but relatively rare in growth hormone (GH) and mixed GH/PRL adenomas. High-mobility group A2 expression was significantly associated with tumor invasion (P<0.05) and was significantly higher in grade IV than in grades I, II, and III adenomas (P<0.05). High levels of high-mobility group A2 expression were more frequently observed in macroadenomas than in microadenomas (P<0.05). High levels of high-mobility group A2 expression also significantly correlated with the proliferation marker Ki-67 (P<0.0001). Real-time quantitative RT-PCR analysis was carried out to evaluate the expression of let-7 in 55 pituitary adenomas. Subsequently, decreased expression of let-7 was confirmed in 23 of 55 (42%) adenomas and was correlated with high-grade tumors (P<0.05). An inverse correlation between let-7 and high-mobility group A2 expression was evident (R=-0.33, P<0.05). These findings support a causal link between let-7 and high-mobility group A2 whereby loss of let-7 expression induces high-mobility group A2 upregulation that represents an important mechanism in pituitary tumorigenesis and progression. (日)
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| ○キーワード (推奨): | 1. | (英) Adenoma (日) (読)
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| 2. | (英) Disease Progression (日) (読)
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| 3. | (英) Female (日) (読)
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| 4. | (英) Gene Expression (日) (読)
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| 5. | (英) HMGA2 Protein (日) (読)
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| 6. | (英) Humans (日) (読)
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| 7. | (英) Immunohistochemistry (日) (読)
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| 8. | (英) Male (日) (読)
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| 9. | (英) MicroRNAs (日) (読)
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| 10. | (英) Pituitary Neoplasms (日) (読)
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| 11. | (英) Reverse Transcriptase Polymerase Chain Reaction (日) (読)
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| 12. | (英) Tumor Markers, Biological (日) (読)
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| 13. | (英) Up-Regulation (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Modern Pathology (United States and Canadian Academy of Pathology)
(pISSN: 0893-3952, eISSN: 1530-0285)
| ○ISSN (任意): | □ | 1530-0285
ISSN: 0893-3952
(pISSN: 0893-3952, eISSN: 1530-0285) Title: Modern pathology : an official journal of the United States and Canadian Academy of Pathology, IncTitle(ISO): Mod PatholPublisher: Springer Nature (NLM Catalog)
(Scopus)
(CrossRef)
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| ○巻 (必須): | □ | 22
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| ○号 (必須): | □ | 3
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| ○頁 (必須): | □ | 431 441
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2009年 1月 9日 (平成 21年 1月 9日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1038/modpathol.2008.202 (→Scopusで検索)
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| ○PMID (任意): | □ | 19136928 (→Scopusで検索)
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| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Pathology, Institute of Health Biosciences, The University of Tokushima Graduate School of Medicine, Tokushima, Japan. zrqian@basic.med.tokushima-u.ac.jp (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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