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Targeted transcriptome profiling of fresh paired normal and tumor tissue samples in glioblastoma patients

ABSTRACT: Glioblastoma (GBM) is the most common and aggressive primary central nervous system malignancy, with median survival of 15 months. Glioblastoma represents extraordinarily high tumor heterogeneity and alterations in genomic, transcriptomic or methylomic levels. To gain deeper insights into the molecular processes involved we studied transcriptome wide expression profiles using RNAseq of normal/tumor tissue pairs of 12 GBM patients and systematically analyzed the differentially expressed genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151352 | GEO | 2020/05/29

REPOSITORIES: GEO

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Multi-omics profiling of paired primary and recurrent glioblastoma patient tissues

Project description:Background Despite maximal therapy with surgery, chemotherapy and radiotherapy, glioblastoma multiforme (GBM) patients have a median survival of only 15 months. Almost all patients inevitably experience symptomatic tumor recurrence. A hallmark of this tumor type is the large heterogeneity between patients and within tumors itself which relate to failure of standardized tumor treatment. In this study, tissue samples of paired primary and recurrent GBM tumors were investigated to identify individual factors related to tumor progression. Methods Paired primary and recurrent GBM tumor tissues from 8 patients were investigated with a multi-omics approach using transcriptomics, proteomics and phosphoproteomics. Results In the studied patient cohort, large variations between and within patients are observed for all omics analyses. A few pathways affected at the different omics levels partly overlapped if patients are analyzed at the individual level, such as synaptogenesis (containing the SNARE complex) and cholesterol metabolism. Phosphoproteomics revealed increased STMN1(S38) phosphorylation that relates to ERBB4 signaling. A pathway tool has been developed to visualize and compare the different omics datasets per patient and showed potential therapeutic drugs, such as abobotulinumtoxina and afatinib, that target these affected pathways. Afatinib targeting ERBB4 signaling is currently in clinical trials for GBM. Conclusions Large variation on all omics levels exist between and within GBM patients. Therefore, it will be rather unlikely to find a drug treatment that would fit all patients. Instead a multi-omics approach can be used to identify affected pathways on the individual patient level and select potential treatment options.

2020-11-17 | PXD017952 | Pride

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Expression data of LN229 cells treated with 23 Pa compressive solid stress (CSS) or no CSS

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Targeted transcriptome profiling of fresh paired normal and tumor tissue samples in glioblastoma patients

Project description:Targeted transcriptome profiling of fresh paired normal and tumor tissue samples in glioblastoma patients

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Project description:Glioblastoma (GBM), the most common and aggressive malignant tumor in adult brain, is a notoriously fatal tumor. For many years, surgical resection and postoperative radiotherapy had been used for the treatment of GBM, which resulted in a poor median survival of about 12 months. Currently, Temozolomide (TMZ) as a clinically meaningful chemotherapy drug has become the standard first-line treatment for GBM, but with an increase of the median survival for about only 2.5 months. In this study, encouraged by previous findings that human astrocytes could be converted into neuronal cells with small molecules and that human GBM cells could be induced into neuronal like cells by transcription factors, we intended to test whether GBM cells could be induced into neuronal like cells by a cocktail of approved drugs and whether this drug cocktail help to suppress GBM in patient derived xenograft (PDX). Here we screened and identified TMZ, Tranilast, and Fasudil, three approved clinical drugs (TTF), to induce GBM cells toward a neuronal fate. Both serum and serum-free cultured GBM cells exhibited neuronal morphology and expressed neuronal genes under TTF treatment. Malignant properties including uncontrolled proliferation and intensive invasion of GBM cells were also attenuated with TTF treatment. Most importantly, when administrated in PDX, TTF cocktail significantly suppressed GBM growth in vivo and prolonged the survival of tumor-bearing mice, as compared to TMZ alone. Our study indicated that using the approved drug cocktail to induce tumor cells toward a neuronal fate might be a clinically promising strategy for GBM treatment.

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Multi-omics profiling of paired primary and recurrent glioblastoma patient tissues

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