Hodgson J Graeme, Yeh Ru-Fang, Ray Amrita, Wang Nicholas J, Smirnov Ivan, Yu Mamie, Hariono Sujatmi, Silber Joachim, Feiler Heidi S, Gray Joe W, Spellman Paul T, Vandenberg Scott R, Berger Mitchel S, James C David
Dept. of Neurological Surgery, University of California, San Francisco, San Francisco, CA, USA.
Neuro Oncol. 2009 Oct;11(5):477-87. doi: 10.1215/15228517-2008-113. Epub 2009 Jan 12.
Development of model systems that recapitulate the molecular heterogeneity observed among glioblastoma multiforme (GBM) tumors will expedite the testing of targeted molecular therapeutic strategies for GBM treatment. In this study, we profiled DNA copy number and mRNA expression in 21 independent GBM tumor lines maintained as subcutaneous xenografts (GBMX), and compared GBMX molecular signatures to those observed in GBM clinical specimens derived from the Cancer Genome Atlas (TCGA). The predominant copy number signature in both tumor groups was defined by chromosome-7 gain/chromosome-10 loss, a poor-prognosis genetic signature. We also observed, at frequencies similar to that detected in TCGA GBM tumors, genomic amplification and overexpression of known GBM oncogenes, such as EGFR, MDM2, CDK6, and MYCN, and novel genes, including NUP107, SLC35E3, MMP1, MMP13, and DDX1. The transcriptional signature of GBMX tumors, which was stable over multiple subcutaneous passages, was defined by overexpression of genes involved in M phase, DNA replication, and chromosome organization (MRC) and was highly similar to the poor-prognosis mitosis and cell-cycle module (MCM) in GBM. Assessment of gene expression in TCGA-derived GBMs revealed overexpression of MRC cancer genes AURKB, BIRC5, CCNB1, CCNB2, CDC2, CDK2, and FOXM1, which form a transcriptional network important for G2/M progression and/or checkpoint activation. Our study supports propagation of GBM tumors as subcutaneous xenografts as a useful approach for sustaining key molecular characteristics of patient tumors, and highlights therapeutic opportunities conferred by this GBMX tumor panel for testing targeted therapeutic strategies for GBM treatment.
构建能够概括多形性胶质母细胞瘤(GBM)肿瘤中所观察到的分子异质性的模型系统,将加速针对GBM治疗的靶向分子治疗策略的测试。在本研究中,我们分析了21个作为皮下异种移植瘤(GBMX)维持的独立GBM肿瘤系中的DNA拷贝数和mRNA表达,并将GBMX分子特征与从癌症基因组图谱(TCGA)获得的GBM临床标本中观察到的特征进行了比较。两个肿瘤组中主要的拷贝数特征均由7号染色体增益/10号染色体缺失所定义,这是一种预后不良的遗传特征。我们还观察到,在与TCGA GBM肿瘤中检测到的频率相似的情况下,已知GBM癌基因如EGFR、MDM2、CDK6和MYCN以及新基因包括NUP107、SLC35E3、MMP1、MMP13和DDX1的基因组扩增和过表达。GBMX肿瘤的转录特征在多次皮下传代过程中是稳定的,其定义为参与M期、DNA复制和染色体组织(MRC)的基因过表达,并且与GBM中预后不良的有丝分裂和细胞周期模块(MCM)高度相似。对源自TCGA的GBM中的基因表达评估显示,MRC癌基因AURKB、BIRC5、CCNB1、CCNB2、CDC2、CDK2和FOXM1过表达,这些基因形成了一个对G2/M进展和/或检查点激活很重要的转录网络。我们的研究支持将GBM肿瘤作为皮下异种移植瘤进行传代培养,这是维持患者肿瘤关键分子特征的一种有用方法,并突出了该GBMX肿瘤组为测试GBM治疗的靶向治疗策略所带来的治疗机会。