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cIMPACT-NOW update 3: recommended diagnostic criteria for "Diffuse astrocytic glioma, IDH-wildtype, with molecular features of glioblastoma, WHO grade IV".cIMPACT-NOW更新3:“弥漫性星形细胞胶质瘤,IDH野生型,具有胶质母细胞瘤分子特征,WHO四级”的推荐诊断标准。
Acta Neuropathol. 2018 Nov;136(5):805-810. doi: 10.1007/s00401-018-1913-0. Epub 2018 Sep 26.
2
Sym004-induced EGFR elimination is associated with profound anti-tumor activity in EGFRvIII patient-derived glioblastoma models.Sym004 诱导的 EGFR 缺失与 EGFRvIII 患者来源的胶质母细胞瘤模型中的抗肿瘤活性密切相关。
J Neurooncol. 2018 Jul;138(3):489-498. doi: 10.1007/s11060-018-2832-6. Epub 2018 Mar 21.
3
Whole Genome Sequencing-Based Discovery of Structural Variants in Glioblastoma.基于全基因组测序的胶质母细胞瘤结构变异发现
Methods Mol Biol. 2018;1741:1-29. doi: 10.1007/978-1-4939-7659-1_1.
4
Protocol for HER2 FISH Using a Non-cross-linking, Formalin-free Tissue Fixative to Combine Advantages of Cryo-preservation and Formalin Fixation.使用非交联、无甲醛组织固定剂进行HER2荧光原位杂交的方案,以结合冷冻保存和甲醛固定的优点。
J Vis Exp. 2017 Dec 25(130):55885. doi: 10.3791/55885.
5
Epidermal growth factor receptor and EGFRvIII in glioblastoma: signaling pathways and targeted therapies.表皮生长因子受体和 EGFRvIII 在胶质母细胞瘤中的作用:信号通路和靶向治疗。
Oncogene. 2018 Mar;37(12):1561-1575. doi: 10.1038/s41388-017-0045-7. Epub 2018 Jan 11.
6
Rindopepimut with temozolomide for patients with newly diagnosed, EGFRvIII-expressing glioblastoma (ACT IV): a randomised, double-blind, international phase 3 trial.里登肽联合替莫唑胺治疗新诊断的表皮生长因子受体VIII 表达型胶质母细胞瘤患者(ACT IV):一项随机、双盲、国际 III 期试验。
Lancet Oncol. 2017 Oct;18(10):1373-1385. doi: 10.1016/S1470-2045(17)30517-X. Epub 2017 Aug 23.
7
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Genes Dev. 2017 Jun 15;31(12):1212-1227. doi: 10.1101/gad.300079.117. Epub 2017 Jul 19.
8
A single dose of peripherally infused EGFRvIII-directed CAR T cells mediates antigen loss and induces adaptive resistance in patients with recurrent glioblastoma.单次外周输注靶向表皮生长因子受体III型变异体(EGFRvIII)的嵌合抗原受体(CAR)T细胞可介导抗原缺失,并在复发性胶质母细胞瘤患者中诱导适应性耐药。
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10
Detection of wild-type EGFR amplification and EGFRvIII mutation in CSF-derived extracellular vesicles of glioblastoma patients.检测脑胶质母细胞瘤患者脑脊液来源的细胞外囊泡中的野生型 EGFR 扩增和 EGFRvIII 突变。
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临床脑胶质瘤样本中检测癌基因扩增和 EGFRvIII 突变状态的实用生物信息学 DNA 测序流程。

Practical Bioinformatic DNA-Sequencing Pipeline for Detecting Oncogene Amplification and EGFRvIII Mutational Status in Clinical Glioblastoma Samples.

机构信息

Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.

Fishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Department of Pathology and Laboratory Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.

出版信息

J Mol Diagn. 2019 May;21(3):514-524. doi: 10.1016/j.jmoldx.2019.02.001. Epub 2019 Apr 15.

DOI:10.1016/j.jmoldx.2019.02.001
PMID:31000415
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6521892/
Abstract

Glioblastoma is a malignant brain tumor with dismal prognosis. Oncogenic mutations in glioblastoma frequently affect receptor tyrosine kinase pathway components that are challenging to quantify because of heterogeneous expression. EGFRvIII, a common oncogenic receptor tyrosine kinase mutant protein in glioblastoma, potentiates tumor malignancy and is an emerging tumor-specific immunotarget, underlining the need for its more accessible and quantitative detection. We used normalized next-generation sequencing data from 117 brain and 371 reference clinical tumor samples to detect focal gene amplifications across the commercial Ion AmpliSeq Cancer Hotspot Panel version 2 and infer EGFRvIII status based on relative coverage dropout of the gene's truncated region within EGFR. In glioblastomas (n = 45), amplification of EGFR [18 (40%)], PDGFRA [3 (7%)], KIT [2 (4%)], MET [1 (2%)], and AKT1 [1 (2%)] was detected. With respect to EGFR and PDGFRA amplification, there was near-complete agreement between next-generation sequencing and in situ hybridization. Consistent with previous reports, this method detected EGFRvIII exclusively in EGFR-amplified glioblastomas [8 (44%)], which was confirmed using long-range PCR. Our study offers a practical method for detecting oncogene amplifications and large intragenic mutations in a clinically implemented hotspot panel that can be quantified using z scores. The validated detection of EGFRvIII using DNA sequencing eliminates problems with transcript degradation, and the provided script facilitates efficient incorporation into a laboratory's bioinformatic pipeline.

摘要

胶质母细胞瘤是一种预后不良的恶性脑肿瘤。胶质母细胞瘤中的致癌突变经常影响受体酪氨酸激酶途径的成分,由于其异质性表达,这些成分难以定量。EGFRvIII 是胶质母细胞瘤中常见的致癌受体酪氨酸激酶突变蛋白,增强了肿瘤的恶性程度,是一种新兴的肿瘤特异性免疫靶点,因此需要更易于获得和定量检测。我们使用来自 117 个脑和 371 个参考临床肿瘤样本的归一化下一代测序数据,在商业 Ion AmpliSeq Cancer Hotspot Panel version 2 上检测整个基因的局灶性基因扩增,并根据 EGFR 中基因截断区域的相对覆盖缺失推断 EGFRvIII 状态。在胶质母细胞瘤(n=45)中,检测到 EGFR[18 个(40%)]、PDGFRA[3 个(7%)]、KIT[2 个(4%)]、MET[1 个(2%)]和 AKT1[1 个(2%)]的扩增。关于 EGFR 和 PDGFRA 扩增,下一代测序和原位杂交之间几乎完全一致。与之前的报道一致,这种方法仅在 EGFR 扩增的胶质母细胞瘤中检测到 EGFRvIII[8 个(44%)],并用长距离 PCR 进行了验证。我们的研究提供了一种实用的方法,用于检测临床实施热点面板中的致癌基因扩增和大型基因内突变,并可使用 z 分数进行定量。使用 DNA 测序验证 EGFRvIII 的检测消除了转录降解的问题,并且提供的脚本有助于将其高效地纳入实验室的生物信息学管道。