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