• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

一种组织特异性转基因小鼠模型显示,癌基因相互作用是胶质瘤发生和进展所必需的。

Oncogene interactions are required for glioma development and progression as revealed by a tissue specific transgenic mouse model.

作者信息

Moore Lynette M, Holmes Kristen M, Fuller Gregory N, Zhang Wei

机构信息

Department of Pathology, the University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Chin J Cancer. 2011 Mar;30(3):163-72. doi: 10.5732/cjc.010.10572.

DOI:10.5732/cjc.010.10572
PMID:21352693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4013312/
Abstract

The aggressive and invasive nature of brain tumors has hampered progress in the design and implementation of efficacious therapies. The recent success of targeted therapies in other tumor types makes this an attractive area for research yet complicating matters is the ability of brain tumors to circumvent the targeted pathways to develop drug resistance. Effective therapies will likely need to target more than one signaling pathway or target multiple nodes within a given pathway. Key to identifying these targets is the elucidation of the driver and passenger molecules within these pathways. Animal models provide a useful tool with many advantages in the study of these pathways. These models provide a means to dissect the critical components of tumorigenesis, as well as serve as agents for preclinical testing. This review focuses on the use of the RCAS/tv-a mouse model of brain tumors and describes their unique ability to provide insight into the role of oncogene cooperation in tumor development and progression.

摘要

脑肿瘤的侵袭性和转移性阻碍了有效治疗方案设计与实施方面的进展。靶向治疗在其他肿瘤类型中的近期成功,使其成为一个颇具吸引力的研究领域,但脑肿瘤规避靶向通路产生耐药性的能力又使情况变得复杂。有效的治疗可能需要针对不止一条信号通路,或针对给定通路内的多个节点。识别这些靶点的关键在于阐明这些通路中的驱动分子和乘客分子。动物模型是研究这些通路的有用工具,具有诸多优势。这些模型提供了剖析肿瘤发生关键成分的方法,还可作为临床前测试的载体。本综述聚焦于脑肿瘤的RCAS/tv-a小鼠模型的应用,并描述了它们在洞察癌基因协同作用在肿瘤发生和发展中的作用方面的独特能力。

相似文献

1
Oncogene interactions are required for glioma development and progression as revealed by a tissue specific transgenic mouse model.一种组织特异性转基因小鼠模型显示,癌基因相互作用是胶质瘤发生和进展所必需的。
Chin J Cancer. 2011 Mar;30(3):163-72. doi: 10.5732/cjc.010.10572.
2
Development of a Sox2 reporter system modeling cellular heterogeneity in glioma.一种模拟胶质瘤细胞异质性的Sox2报告系统的开发。
Neuro Oncol. 2015 Mar;17(3):361-71. doi: 10.1093/neuonc/nou320. Epub 2014 Nov 21.
3
RCAS-TVA in the mammary gland: an in vivo oncogene screen and a high fidelity model for breast transformation?乳腺中的RCAS-TVA:一种体内癌基因筛选及乳腺转化的高保真模型?
Cell Cycle. 2007 Apr 1;6(7):823-6. doi: 10.4161/cc.6.7.4074. Epub 2007 Apr 22.
4
The c-myc and PyMT oncogenes induce different tumor types in a somatic mouse model for pancreatic cancer.在胰腺癌的体细胞小鼠模型中,c-myc和PyMT癌基因会诱导产生不同类型的肿瘤。
Genes Dev. 2003 Dec 15;17(24):3127-38. doi: 10.1101/gad.1140403. Epub 2003 Dec 17.
5
Genetically engineered mouse models of brain cancer and the promise of preclinical testing.脑癌的基因工程小鼠模型及临床前测试的前景。
Brain Pathol. 2009 Jan;19(1):132-43. doi: 10.1111/j.1750-3639.2008.00234.x.
6
Animal models of melanoma: a somatic cell gene delivery mouse model allows rapid evaluation of genes implicated in human melanoma.黑色素瘤动物模型:一种体细胞基因递送小鼠模型可快速评估与人类黑色素瘤相关的基因。
Chin J Cancer. 2011 Mar;30(3):153-62. doi: 10.5732/cjc.011.10007.
7
Insulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.胰岛素样生长因子结合蛋白 2 驱动的神经胶质瘤进展可通过阻断临床意义重大的整合素、整合素连接激酶和 NF-κB 网络来预防。
Proc Natl Acad Sci U S A. 2012 Feb 28;109(9):3475-80. doi: 10.1073/pnas.1120375109. Epub 2012 Feb 15.
8
Use of avian retroviral vectors to introduce transcriptional regulators into mammalian cells for analyses of tumor maintenance.使用禽逆转录病毒载体将转录调节因子导入哺乳动物细胞以分析肿瘤维持。
Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8764-9. doi: 10.1073/pnas.1133333100. Epub 2003 Jul 11.
9
Rapid and robust transgenic high-grade glioma mouse models for therapy intervention studies.用于治疗干预研究的快速且稳健的转基因高级别神经胶质瘤小鼠模型。
Clin Cancer Res. 2010 Jul 1;16(13):3431-41. doi: 10.1158/1078-0432.CCR-09-3414. Epub 2010 May 14.
10
A Cre-loxP-based mouse model for conditional somatic gene expression and knockdown in vivo by using avian retroviral vectors.一种基于Cre-loxP的小鼠模型,用于通过禽逆转录病毒载体在体内进行条件性体细胞基因表达和基因敲低。
Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):10137-42. doi: 10.1073/pnas.0800487105. Epub 2008 Jul 11.

引用本文的文献

1
Insulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.胰岛素样生长因子结合蛋白 2 驱动的神经胶质瘤进展可通过阻断临床意义重大的整合素、整合素连接激酶和 NF-κB 网络来预防。
Proc Natl Acad Sci U S A. 2012 Feb 28;109(9):3475-80. doi: 10.1073/pnas.1120375109. Epub 2012 Feb 15.

本文引用的文献

1
p27 deficiency is associated with migration defects in PDGF-expressing gliomas in vivo.p27 缺乏与体内表达 PDGF 的神经胶质瘤迁移缺陷有关。
Cell Cycle. 2010 Apr 15;9(8):1562-7. doi: 10.4161/cc.9.8.11259.
2
Preclinical evaluation of radiation and perifosine in a genetically and histologically accurate model of brainstem glioma.脑干部位神经胶质瘤的基因和组织学精确模型中的放射治疗与培菲替尼的临床前评估。
Cancer Res. 2010 Mar 15;70(6):2548-57. doi: 10.1158/0008-5472.CAN-09-2503. Epub 2010 Mar 2.
3
Defective DNA double-strand break repair underlies enhanced tumorigenesis and chromosomal instability in p27-deficient mice with growth factor-induced oligodendrogliomas.
p27 缺陷小鼠在生长因子诱导的少突胶质细胞瘤中,由于 DNA 双链断裂修复缺陷,肿瘤发生和染色体不稳定性增强。
Oncogene. 2010 Mar 25;29(12):1720-31. doi: 10.1038/onc.2009.465. Epub 2010 Jan 11.
4
Activated BRAF induces gliomas in mice when combined with Ink4a/Arf loss or Akt activation.激活的 BRAF 与 Ink4a/Arf 缺失或 Akt 激活联合可诱导小鼠发生神经胶质瘤。
Oncogene. 2010 Jan 21;29(3):335-44. doi: 10.1038/onc.2009.333. Epub 2009 Oct 26.
5
IGFBP2 is a candidate biomarker for Ink4a-Arf status and a therapeutic target for high-grade gliomas.胰岛素样生长因子结合蛋白2(IGFBP2)是一种与Ink4a-Arf状态相关的候选生物标志物,也是高级别胶质瘤的治疗靶点。
Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16675-9. doi: 10.1073/pnas.0900807106. Epub 2009 Sep 16.
6
The PTEN-regulating microRNA miR-26a is amplified in high-grade glioma and facilitates gliomagenesis in vivo.调控PTEN的微小RNA miR-26a在高级别胶质瘤中扩增,并在体内促进胶质瘤的发生。
Genes Dev. 2009 Jun 1;23(11):1327-37. doi: 10.1101/gad.1777409.
7
Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma.少突胶质前体细胞可作为实验性胶质瘤的起源细胞。
Oncogene. 2009 Jun 11;28(23):2266-75. doi: 10.1038/onc.2009.76. Epub 2009 Apr 27.
8
Comparative analysis of DNA repair in stem and nonstem glioma cell cultures.胶质瘤干细胞与非干细胞培养物中DNA修复的比较分析。
Mol Cancer Res. 2009 Mar;7(3):383-92. doi: 10.1158/1541-7786.MCR-08-0409. Epub 2009 Mar 10.
9
Plasma IGFBP-2 levels predict clinical outcomes of patients with high-grade gliomas.血浆胰岛素样生长因子结合蛋白-2水平可预测高级别胶质瘤患者的临床预后。
Neuro Oncol. 2009 Oct;11(5):468-76. doi: 10.1215/15228517-2008-114. Epub 2009 Jan 22.
10
Genetically engineered mouse models of brain cancer and the promise of preclinical testing.脑癌的基因工程小鼠模型及临床前测试的前景。
Brain Pathol. 2009 Jan;19(1):132-43. doi: 10.1111/j.1750-3639.2008.00234.x.