TGFα, c-MYC, mutated CTNNB1 and their combinations act distinctly on the Hep3B tumors in nude mice

• Material Type: 博士論文
• ISSN: 00306169
• Title: TGFα, c-MYC, mutated CTNNB1 and their combinations act distinctly on the Hep3B tumors in nude mice
• Author/Editor: Noritake, Hidenao
• Author Heading: Noritake, Hidenao
• Publication, Distribution, etc.: 大阪大学医学部
• Publication Date: 2014
• Publication Date (W3CDTF): 2014
• Alternative Title: TGFα,c-MYC，変異型CTNNB1遺伝子およびこれらの組み合わせはヌードマウスにおけるHep3B腫瘍形成に明確に作用する
• Periodical title: Medical Journal of Osaka University
• Degree grantor/type: 浜松医科大学
• Date Granted: 2014-03-17
• Date Granted (W3CDTF): 2014-03-17
• Dissertation Number: 甲第668号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 13802甲第668号
• Text Language Code: eng
• Subject Heading: TGFα; C-MYC; mutant CTNNB1; HCC; apoptosis; transdifferentiation
• Target Audience: 一般
• Note (General): doctoral; 医学系研究科; Hepatocellular carcinoma (HCC) is the most common hepatic tumor worldwide and is a major cause of death in many countries. Although chronic viral infections and hepatotoxic agents are the major risk factors, the molecular pathogenesis of HCC remains largely unknown. Among model mice, TGFα/c-Myc transgenic mice develop human HCC-like tumors. Whole genome sequencing of HCC tumors from patients has shown that mutations to CTNNB1 (β-catenin) are the most frequent (15.9%). So in this study, we characterized the effects of TGFα, c-MYC and mutant CTNNB1 genes on the transplantable Hep3B cells. TGFα increased the tumor number after transplanting Hep3B cells. Mutant CTNNB1 changed the characteristics of Hep3B tumor cells into a disarranged structure with loose cell-cell contacts. And co-transduction of TGFα and mutant CTNNB1 synergistically increased the growth rate, size and weight of Hep3B tumors. Unexpectedly, c-MYC overexpression in the Hep3B cells induced apoptosis. Interestingly, TGFα+mutant CTNNB1+MYC-transduced cells grew very slowly and the tumor showed transdifferentiation into a cholangial duct. These results suggest that the interaction of these three genes determines the characteristics of Hep3B tumor. Overexpression of c-MYC by a lentivirus in c-MYC-upregulated HCC tumors might be used as a molecular targeted therapy.
• Persistent ID (NDL): info:ndljp/pid/8953199; https://dl.ndl.go.jp/pid/8953199
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Available (W3CDTF): 2015-03-03
• Date Accepted (W3CDTF): 2015-02-03T05:25:05+09:00
• Date Created (W3CDTF): 2018-08-27
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10271/2789; https://hama-med.repo.nii.ac.jp/records/2671
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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