Next generation sequencing from primary glioblastoma patient tissues (Total RNA-seq)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE255626 | GEO | 2026/01/21
REPOSITORIES: GEO
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Project description:Although multi-omics studies of glioblastoma (GBM) have improved understanding of its biology nature and accelerated targeted therapy, data for paired adjacent normal tissues remains limited. Here, we report transcriptomes from 2 paired and 1 non-paired tumor and adjacent normal tissues (NAT) of glioblastoma (GBM) patients sequenced using Illumina Novaseq platform, and 150 bp paired-end reads were generated. This dataset provides a resource of paired GBM and normal tissues to identify novel tumor-specific oncogenes or tumor-suppressor genes.
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Project description:Next generation sequencing from primary glioblastoma patient tissues (Total RNA-seq)
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Project description:Samples were obtained from 52 non-recurrent GBM patients treated at Severance Hospital
2019-05-29 | GSE131837 | GEO
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.
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Project description:Although multi-omics studies of glioblastoma (GBM) have improved understanding of its biology nature and accelerated targeted therapy, data for paired adjacent normal tissues (NAT) remains limited. Here, we report proteomes from 3 paired of tumor tissues and NATs of glioblastoma (GBM) patients using liquid chromatography with tandem mass spectrometry (LC-MS/MS)-based label-free quantification. This dataset provides a resource of paired GBM and normal tissues to identify novel tumor-specific oncogenes or tumor-suppressor genes.
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Project description:Glioblastoma (GBM) stem cells (GSCs) are largely associated with a poor prognosis of GBM. Although the importance of identifying and validating molecular markers in GBM has been emphasized, single markers covering all GSCs are lacking. Through in vitro antibody screening, in this study, we demonstrated that CD97 identifies GSCs as a novel surface marker. Compared to conventional well-known GSC markers, such as CD133, CD44 and CD15, only CD97 was notably detected in all tested patient-derived GSCs. GBM patients expressing high levels of CD97 experienced worse clinical outcomes, and were predictive of poor overall survival in the public database. CD97 is required for GSC proliferation and self-renewal and was shown to reduce mouse survival with aggressive tumor progression in an orthotopic xenograft model. A comparative transcriptomic analysis revealed that CD97 triggers mTORC2 signaling through Akt (S473) phosphorylation, enhancing the expression of downstream genes, including ARHGAP1, BZW1, and BZW2. Moreover, inhibition of mTORC2 signaling with the pharmacological inhibitor JR-AP2-011 suppressed GSC proliferation, self-renewal, and downstream gene expression. Furthermore, sorting of CD97-enriched cells from patient-derived GSCs revealed that CD97 promotes GSC self-renewal and tumorigenicity via mTORC2/AKT signaling. Thus, our findings suggest that CD97 may be a general GSC enrichment marker in GBM and that the CD97-related pathway might serve as a therapeutic target for GBM.
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