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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 we...
ORGANISM(S): Homo sapiens 
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 ...
ORGANISM(S): Homo sapiens 
Genomically amplified Akt3 activates DNA repair pathway and promotes glioma progression
Glioblastoma cell lines were xenografted onto mice and resulting tumors were profiled by microarray. Xenograft recipient mice were NOD/SCID/gamma (NSG) male mice 3 months old. In this set, 6 total samples were analyzed. There were three biological replicates for each of two conditions: EGFRvIII co...
ORGANISM(S): Homo sapiens 
The mTOR-allosteric inhibitor, RAD001, in combination with a PI3K/mTOR ATP-site competitive inhibitor, BEZ235, causes gene reprogramming, autophagy and tumor regression, in a mouse model approximating human HCC with poor prognosis, leading to an investigator Phase 1B-2 clinical trial. Comparative st...
ORGANISM(S): Mus musculus 
Epidermal Growth Factor Receptor (EGFR) gene amplification and mutations are the most common oncogenic events in Glioblastoma (GBM), but the mechanisms by which they promote aggressive tumor growth are not well understood. Here, through integrated epigenome and transcriptome analyses of cell lines, ...
ORGANISM(S): Homo sapiens 
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