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Learn MoreThe goal of this study is to identify the pathway alterations driving the adaptive resistance to PI3K inhibition in GBM. We generated the resistant cell lines through a patient-derived in vivo glioma sphere-forming cell (GSC) model. We performed RNA-seq on the paired GSC samples including the parental and resistant groups. Libraries were sequenced with an average coverage for each tumor of 50x on the Hiseq4000 platform from Illumina, using 76 nt pair-ended reads. RNA-seq raw data were pre-processed using PRADA. PRADA aligned RNA-seq reads to a composite reference database composed of whole genome and transcriptome sequences; we used the hg19 human genome assembly, together with the Ensembl64 transcriptome version. Transcripts were filtered for size and protein-coding genes. Expression data were normalized to reads per kilobase per million reads, and these values were log2-transformed for further analyses. SOURCE: Dimpy Koul (dkoul@mdanderson.org) - MD Anderson Cancer Center
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