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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 嚴震東(Chen-Tung Yen) | |
dc.contributor.author | Nai-Wei Yao | en |
dc.contributor.author | 姚乃維 | zh_TW |
dc.date.accessioned | 2021-06-15T12:29:41Z | - |
dc.date.available | 2017-08-24 | |
dc.date.copyright | 2016-08-24 | |
dc.date.issued | 2016 | |
dc.date.submitted | 2016-08-05 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/50099 | - |
dc.description.abstract | 神經膠質瘤(gliomas)是腦部常見的惡性腫瘤,即使經過治療,神經膠質瘤的病人仍有很差的預後。為更了解神經膠質瘤的病程發展以及治療後腫瘤生長情形,本論文致力於提出一個嶄新的觀察策略,以活體多參數磁振造影技術結合離體分析,建立功能性評估神經膠質瘤之病程發展。本論文中分為三個部分,分別就分子層面、細胞及其腫瘤生長環境,以及幹細胞治療療效之觀察,來展示此功能性評估策略之重要性與必要性。
第一個部分利用骨橋素(osteopontin, OPN)作為標準分子,以活體多參數核磁共振造影技術結合離體分子與細胞分析方法,來綜合評估神經膠質瘤之生長情形。骨橋素是促進癌症共同特徵(the hallmarks of cancer)的關鍵因子,在細胞增生、血管新生以及腫瘤細胞之代謝上扮演重要角色。利用此綜合評估策略,可了解骨橋素和其他促進腫瘤生長的關鍵因子在神經膠質瘤病程發展上的重要性。第二部分,我們利用此功能性評估策略來觀察腫瘤生長環境如何影響神經膠質瘤的惡性程度,並進一步展示巨噬細胞的極化與分化是影響腫瘤惡性程度的重要因素。在腫瘤生長環境中,不同亞型的巨噬細胞將會影響該腫瘤的惡性程度,此發現將會對未來腫瘤標靶治療有所助益。由於傳統治療方法,如手術、放射線治療與化學療法等,對於神經膠質瘤並沒有顯著的治療效果,近年來,各種新興的療法不斷被研究者們所提出,因此,如何有效評估新興療法之成效是相當重要的議題。於本論文的第三部分,我們以核磁共振造影結合免疫組織染色,來觀察神經幹細胞療法對於神經膠質瘤生長的影響與變化,並評估此治療方法對於神經膠質瘤之療效。 本論文中所提出的功能性評估策略,在多個層面上都展示了其應用性與重要性,結合活體核磁共振造影技術與離體分析方法,能提供更多資訊進一步了解神經膠質瘤之病程發展,並有效的評估新興療法之成效,對於未來治療發展能有所貢獻。 | zh_TW |
dc.description.abstract | Gliomas are aggressive brain tumors with poor prognosis and remain refractory to treatment. The purpose of this dissertation is providing a novel approach combining in vivo multi-parametric magnetic resonance imaging (MRI) and immunohistochemistry, with the assistance of in vitro cell culture assessments, to monitor the pathogenic development of gliomas. Three inter-related studies are included in this dissertation. The first part is to use osteopontin (OPN) as a model molecule to establish functional assessment of glioma pathogenesis using multi-parametric MRI combined with in vitro analyses, which can be further applied to assess the functional roles of other driver genes in promoting cancer hallmarks related to proliferation, angiogenesis and altered metabolism. In the second study, the multi-parametric MRI methods were performed to demonstrate the role of host microenvironment in dictating the aggressiveness of gliomas, through differential programming of tumor-associated macrophages. We show that the differential polarization of glioma-associated macrophages (GAMs) into M1 or M2 subtypes in different host microenvironments is associated with aggressive phenotypes of gliomas, suggesting that macrophage programming plays an important role in glioma development and that targeting GAMs may serve as a promising therapeutic approach. The third part is to combine T2-weighted MRI and immunohistochemical analyses to evaluate the effects of targeted migration of neural stem/progenitor cells (NSPCs) on tumor development in N-ethyl-N-nitrosourea (ENU)-induced rat brain tumor model. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T12:29:41Z (GMT). No. of bitstreams: 1 ntu-105-F99B41012-1.pdf: 5979183 bytes, checksum: e91bcbd6d95008dab2e29aaef61f3304 (MD5) Previous issue date: 2016 | en |
dc.description.tableofcontents | 口試委員會審定書 #
誌謝 i 中文摘要 ii ABSTRACT iii CONTENTS iv LIST OF FIGURES viii LIST OF TABLES x Chapter 1 Background 1 1.1 Glioblastoma 1 1.2 The hallmarks of cancer 1 1.3 Key molecular player involved in cancer hallmarks 2 1.4 Tumor microenvironment 3 1.4.1 Endothelium and tumor angiogenesis 4 1.4.2 Tumor-associated macrophages (TAMs) and tumor malignancy 5 1.4.3 Neural stem/progenitor cells (NSPCs) and stem cell therapy 6 1.5 Multi-parametric magnetic resonance imaging (MRI) 7 1.5.1 Anatomical and structural assessments of MRI 8 1.5.2 Metabolic and functional assessments of MRI 9 1.6 Motivation and Purposes 11 Chapter 2 Functional assessment of glioma pathogenesis by in vivo multi-parametric magnetic resonance imaging and in vitro analyses: the key molecular player osteopontin (OPN) 13 2.1 Introduction 13 2.2 Materials and Methods 15 2.2.1 Antibodies and cell line 15 2.2.2 Lentivirus-based shRNA KD approach 16 2.2.3 Western blot analysis 16 2.2.4 Cell viability, proliferation, apoptosis and colony formation assays 16 2.2.5 In vivo rat C6 glioma model 17 2.2.6 Multi-parametric magnetic resonance imaging (MRI) methods 18 2.2.7 Histological examination 20 2.2.8 Statistical Analysis 20 2.3 Results 21 2.3.1 KD of OPN expression reduces C6 glioma cell viability, proliferation, survival, and clonogenicity 21 2.3.2 KD of OPN expression reduces tumor growth and prolongs survival in rat glioma model 22 2.3.3 OPN deficiency is associated with decreased glioma malignancies 22 2.3.4 KD of OPN suppresses tumor angiogenesis 24 2.3.5 KD of OPN expression is associated with changes in tumor-associated metabolites 25 2.4 Discussion 33 Chapter 3 Differential macrophage programming is associated with aggressiveness of gliomas 39 3.1 Introduction 39 3.2 Materials and Methods 42 3.2.1 Antibodies and cell line 42 3.2.2 In vivo rat C6 glioma model 42 3.2.3 Multi-parametric magnetic resonance imaging (MRI) methods 43 3.2.4 Histological examination 45 3.2.5 Statistical Analysis 45 3.3 Results 45 3.3.1 Different host microenvironment influences rat C6 glioma growth and animal survival 45 3.3.2 Host microenvironment influences angiogenesis of C6 gliomas in Wistar and SD rats 46 3.3.3 Abundant tumor-associated macrophages (TAMs) located in C6 gliomas in both SD and Wistar rats 47 3.3.4 TAMs in C6 gliomas in both rats are monocyte-derived macrophages from peripheral blood 48 3.3.5 Different programming of tumor-associated macrophages (TAMs) is associated with aggressive phenotypes in C6 gliomas 49 3.3.6 The induction signals of M1 or M2 subtypes of TAM in C6 gliomas in SD and Wistar rats 50 3.4 Discussion 57 Chapter 4 Promoted growth of brain tumor with severe hemorrhage by the transplantation of neural stem/progenitor cells facilitated by CXCL12 62 4.1 Introduction 62 4.2 Materials and Methods 64 4.2.1 Animals 64 4.2.2 The ENU-induced brain tumor model 65 4.2.3 Harvesting and culturing of primary GFP-NSPCs 65 4.2.4 GFP-NSPC implantation and local CXCL12 administration 66 4.2.5 Magnetic resonance imaging 66 4.2.6 Data analysis 67 4.2.7 Histological examination 67 4.2.8 Statistical analysis 68 4.3 Results 69 4.3.1 The combination of CXCL12 and GFP-NSPCs promotes ENU-induced brain-tumor growth 69 4.3.2 The combination of CXCL12 and GFP-NSPCs increases the severity of intratumoral hemorrhage 69 4.3.3 Increased CXCL12 and CXCR4 expression following combined GFP-NSPC and CXCL12 treatments 70 4.3.4 Histological evidence of GFP-NSPC-targeted migration into the glioma region 70 4.3.5 Phenotypic characterization of GFP-NSPCs 71 4.4 Discussion 78 Chapter 5 Discussion and Conclusion 82 5.1 Discussion 82 5.2 Conclusion 85 5.3 Future works 85 Reference 87 Abbreviation 100 Honors and Publications 102 | |
dc.language.iso | en | |
dc.title | 以活體多參數磁振造影技術結合離體分析建立功能性評估神經膠質瘤之病程發展 | zh_TW |
dc.title | Functional assessment of glioma pathogenesis by in vivo multi-parametric magnetic resonance imaging and in vitro analyses | en |
dc.type | Thesis | |
dc.date.schoolyear | 104-2 | |
dc.description.degree | 博士 | |
dc.contributor.coadvisor | 張程(Chen Chang),張久瑗(Jeou-Yuan Chen) | |
dc.contributor.oralexamcommittee | 莊偉哲(Woei-Jer Chuang),黃國書(Guo-Shu Huang),洪東源(Dueng-Yuan Hueng),邱正迪(Cheng-Di Chiu) | |
dc.subject.keyword | 核磁共振造影,骨橋素,巨噬細胞,腫瘤生成,神經幹細胞療法, | zh_TW |
dc.subject.keyword | MRI,OPN,macrophage,tumorigenesis,stem cell therapy, | en |
dc.relation.page | 103 | |
dc.identifier.doi | 10.6342/NTU201601943 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2016-08-05 | |
dc.contributor.author-college | 生命科學院 | zh_TW |
dc.contributor.author-dept | 生命科學系 | zh_TW |
顯示於系所單位: | 生命科學系 |
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