• 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

相似文献

1
Primary and secondary glioblastomas: from concept to clinical diagnosis.原发性和继发性胶质母细胞瘤:从概念到临床诊断
Neuro Oncol. 1999 Jan;1(1):44-51. doi: 10.1093/neuonc/1.1.44.
2
Roles of the functional loss of p53 and other genes in astrocytoma tumorigenesis and progression.p53及其他基因功能丧失在星形细胞瘤发生发展中的作用。
Neuro Oncol. 1999 Apr;1(2):124-37. doi: 10.1093/neuonc/1.2.124.
3
Phenotype vs genotype in the evolution of astrocytic brain tumors.星形细胞瘤演变过程中的表型与基因型
Toxicol Pathol. 2000 Jan-Feb;28(1):164-70. doi: 10.1177/019262330002800121.
4
Genetic profile of gliosarcomas.胶质肉瘤的基因图谱。
Am J Pathol. 2000 Feb;156(2):425-32. doi: 10.1016/S0002-9440(10)64746-3.
5
Primary glioblastomas with and without EGFR amplification: relationship to genetic alterations and clinicopathological features.原发性胶质母细胞瘤伴或不伴 EGFR 扩增:与遗传改变和临床病理特征的关系。
Neuropathology. 2010 Aug;30(4):392-400. doi: 10.1111/j.1440-1789.2009.01081.x. Epub 2009 Dec 16.
6
Genetic pathways to primary and secondary glioblastoma.原发性和继发性胶质母细胞瘤的遗传途径。
Am J Pathol. 2007 May;170(5):1445-53. doi: 10.2353/ajpath.2007.070011.
7
Mutations of TP53, amplification of EGFR, MDM2 and CDK4, and deletions of CDKN2A in malignant astrocytomas.恶性星形细胞瘤中TP53的突变、EGFR、MDM2和CDK4的扩增以及CDKN2A的缺失。
Pol J Pathol. 1998;49(4):267-71.
8
Alterations of cell cycle regulatory genes in primary (de novo) and secondary glioblastomas.原发性(新发)和继发性胶质母细胞瘤中细胞周期调控基因的改变。
Acta Neuropathol. 1997 Oct;94(4):303-9. doi: 10.1007/s004010050711.
9
Correlation among pathology, genotype, and patient outcomes in glioblastoma.胶质母细胞瘤的病理学、基因型与患者预后之间的相关性。
J Neuropathol Exp Neurol. 2006 Sep;65(9):846-54. doi: 10.1097/01.jnen.0000235118.75182.94.
10
Overexpression of the EGF receptor and p53 mutations are mutually exclusive in the evolution of primary and secondary glioblastomas.表皮生长因子受体的过表达与p53突变在原发性和继发性胶质母细胞瘤的发展过程中相互排斥。
Brain Pathol. 1996 Jul;6(3):217-23; discussion 23-4. doi: 10.1111/j.1750-3639.1996.tb00848.x.

引用本文的文献

1
Physical activity and glioblastoma: a paradigm shift in neuro-oncology therapy.体育活动与胶质母细胞瘤:神经肿瘤学治疗的范式转变
Front Oncol. 2025 Jul 30;15:1638060. doi: 10.3389/fonc.2025.1638060. eCollection 2025.
2
Glioblastoma: Overview of Proteomic Investigations and Biobank Approaches for the Development of a Multidisciplinary Translational Network.胶质母细胞瘤:蛋白质组学研究及生物样本库方法概述,用于构建多学科转化网络
Cancers (Basel). 2025 Jun 26;17(13):2151. doi: 10.3390/cancers17132151.
3
Neurocognitive function and health-related quality of life among glioblastoma patients: A prospective study.胶质母细胞瘤患者的神经认知功能与健康相关生活质量:一项前瞻性研究。
J Public Health Afr. 2025 Jan 10;16(1):660. doi: 10.4102/jphia.v16i1.660. eCollection 2025.
4
Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.胶质母细胞瘤中的肿瘤异质性与耐药性:干细胞的作用
Apoptosis. 2025 May 15. doi: 10.1007/s10495-025-02123-y.
5
Gut microbiota and their influence in brain cancer milieu.肠道微生物群及其在脑癌微环境中的影响。
J Neuroinflammation. 2025 May 1;22(1):129. doi: 10.1186/s12974-025-03434-2.
6
Proton beam therapy in a patient with secondary glioblastoma (32 years after postoperative irradiation of medulloblastoma): case report and literature review.质子束治疗继发性胶质母细胞瘤患者(髓母细胞瘤术后放疗 32 年后):病例报告及文献复习。
Radiat Oncol. 2024 Oct 5;19(1):136. doi: 10.1186/s13014-024-02515-5.
7
Recent Advances in Marine-Derived Nanoformulation for the Management of Glioblastoma.用于胶质母细胞瘤治疗的海洋来源纳米制剂的最新进展
Mol Biotechnol. 2024 Sep 26. doi: 10.1007/s12033-024-01287-3.
8
Integrated Gene Expression Data-Driven Identification of Molecular Signatures, Prognostic Biomarkers, and Drug Targets for Glioblastoma.基于整合基因表达数据的胶质母细胞瘤分子特征、预后生物标志物和药物靶点的鉴定。
Biomed Res Int. 2024 Aug 16;2024:6810200. doi: 10.1155/2024/6810200. eCollection 2024.
9
Gene expression profiling and the isocitrate dehydrogenase mutational landscape of temozolomide‑resistant glioblastoma.替莫唑胺耐药性胶质母细胞瘤的基因表达谱及异柠檬酸脱氢酶突变图谱
Oncol Lett. 2024 Jun 17;28(2):378. doi: 10.3892/ol.2024.14511. eCollection 2024 Aug.
10
Integrative spatial analysis reveals a multi-layered organization of glioblastoma.整合空间分析揭示胶质母细胞瘤的多层次组织。
Cell. 2024 May 9;187(10):2485-2501.e26. doi: 10.1016/j.cell.2024.03.029. Epub 2024 Apr 22.

原发性和继发性胶质母细胞瘤:从概念到临床诊断

Primary and secondary glioblastomas: from concept to clinical diagnosis.

作者信息

Kleihues P, Ohgaki H

机构信息

International Agency for Research on Cancer (IARC), World Health Organization (WHO), Lyon, France.

出版信息

Neuro Oncol. 1999 Jan;1(1):44-51. doi: 10.1093/neuonc/1.1.44.

DOI:10.1093/neuonc/1.1.44
PMID:11550301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1919466/
Abstract

Glioblastomas may develop de novo (primary glioblastomas) or through progression from low-grade or anaplastic astrocytomas, (secondary glioblastomas). These subtypes of glioblastoma constitute distinct disease entities that evolve through different genetic pathways, affect patients at different ages, and are likely to differ in prognosis and response to therapy. Primary glioblastomas develop in older patients and typically show EGFR overexpression, PTEN (MMAC1) mutations, CDKN2A (p16) deletions, and less frequently, MDM2 amplification. Secondary glioblastomas develop in younger patients and often contain TP53 mutations as the earliest detectable alteration. These characteristics are derived largely from patients selected on the basis of clinical history and sequential biopsies. Currently available data are insufficient for a substitution of histologic classification and grading of astrocytic tumors by genetic typing alone. More subtypes of glioblastomas may exist with intermediate clinical and genetic profiles, a factor exemplified by the giant-cell glioblastoma that clinically and genetically occupies a hybrid position between primary (de novo) and secondary glioblastomas. Future research should aim at the identification of criteria for a combined clinical, histologic, and genetic classification of astrocytic tumors.

摘要

胶质母细胞瘤可原发形成(原发性胶质母细胞瘤),或由低级别或间变性星形细胞瘤进展而来(继发性胶质母细胞瘤)。这些胶质母细胞瘤亚型构成了不同的疾病实体,它们通过不同的遗传途径演变,影响不同年龄段的患者,并且在预后和对治疗的反应方面可能存在差异。原发性胶质母细胞瘤发生于老年患者,通常表现为表皮生长因子受体(EGFR)过表达、第10号染色体同源缺失性磷酸酶-张力蛋白基因(PTEN,又称MMAC1)突变、细胞周期蛋白依赖性激酶抑制剂2A基因(CDKN2A,又称p16)缺失,较少见的还有鼠双微体2基因(MDM2)扩增。继发性胶质母细胞瘤发生于年轻患者,通常最早可检测到的改变是含有第17号染色体短臂上的肿瘤抑制基因(TP53)突变。这些特征很大程度上源自根据临床病史和序贯活检选择的患者。目前可获得的数据不足以仅通过基因分型替代星形细胞瘤的组织学分类和分级。可能存在更多具有中间临床和基因特征的胶质母细胞瘤亚型,巨大细胞胶质母细胞瘤在临床和遗传学上处于原发性(新发)和继发性胶质母细胞瘤之间的混合位置就是一个例证。未来的研究应致力于确定星形细胞瘤临床、组织学和基因联合分类的标准。