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Copy number variation comparison between control and CC214-2 resistant GBM39 xenografts

ABSTRACT: Here we present genome-wide copy number variation data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing the absence of significant differences between the two groups, demonstrating that resistance to CC214-2 is due to adaptation rather than gene mutations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53042 | GEO | 2013/12/06

SECONDARY ACCESSION(S): PRJNA230729

REPOSITORIES: GEO

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Copy number variation comparison between control and CC214-2 resistant GBM39 xenografts

Project description:Here we present genome-wide copy number variation data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing the absence of significant differences between the two groups, demonstrating that resistance to CC214-2 is due to adaptation rather than gene mutations. The genomic DNA extracted from the 4 xenografts samples was analysed with genome-wide Affymetrix SNP6.0 array

2013-12-06 | E-GEOD-53042 | biostudies-arrayexpress

Gene Expression analysis comparison between control and CC214-2 resistant GBM39 xenografts

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Gene Expression analysis comparison between control and CC214-2 resistant GBM39 xenografts

Project description:Here we present gene expression analysis data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing that the expressioin profiles of 88 genes are significantly different between the two groups. GBM39 primary neurospheres were cultured in standard cancer stem cell medium conditions and then were injected in the mice flanks to generate xenograft tissues. Mice carrying CC214-2 resistant xenografts were treated with a solution of CC214-2 once every two days, by gavage, for 40 days. Total RNA was extracted from GBM39 control and CC214-2 resistant xenografts using the Qiagen RNA micro kit protocol and analysed by Affymetrix U133 plus 2.0 array

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Project description:Copy number analysis of human GBM samples were performed, and a high frequency of deletions of the PTPRD gene on chromosome 9p23-24.1 were identified. Keywords: SNP microarray, glioblastoma multiforme, copy number, amplification, deletion Genomic DNA from 58 GBM tumor samples were hybridized to Affymetrix 250K NspI Gene Chip Arrays and analyzed by dChip using the hg17 genome assembly.

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SNP copy number data from glioblastoma subcutaneous xenografts

Project description:Development of model systems that recapitulate the molecular heterogeneity observed amongst 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 GBMs 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. In conclusion, 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. Disease state analysis

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