Glioblastoma(GBM) tissues: Tumor tissues(C) vs. Normal tissues(N)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE109569 | GEO | 2018/12/26
REPOSITORIES: GEO
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Project description:glioblastoma(GBM) tissues: Tumor tissues(C) vs. Normal tissues(N)
| PRJNA431408 | ENA
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.
2021-09-24 | PXD028730 |
Project description:We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation. Keywords: comparative genomic hybridization
2008-04-29 | GSE9177 | GEO
Project description:We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation. Keywords: comparative genomic hybridization DNA copy number abberation of human glioblastoma tumors were obtained by comparative genomic hybridization of GBM tumor vs. normal human DNA. 11 human GBM samples were analyzed on Agilent human 244A human cgh array (G4411B). Normal Human DNA was used as reference. Some samples were hybridized with dye-swap replica.
2008-04-29 | E-GEOD-9177 | biostudies-arrayexpress
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.
2023-10-01 | GSE184643 | GEO
Project description:This microarray contains expression data for two GBM tissue samples, four GSC cultures grown as spheres and one NFC culture grown as spheres Total RNA was isolated from GSC cultures and GBM tissues
2015-11-26 | E-GEOD-60705 | biostudies-arrayexpress
Project description:We used microarrays to investigate the whole genome gene expression level changes of LncRNAs in human Glioblastoma multiforme (GBM) and normal brain tissues, and try to find out some LncRNA associated with the tumorigenesis of GBM. The human LncRNA microarray analysis of 9 samples (5 GBM and 4 normal brain tissues) were completed. Total RNA from each sample was quantified and RNA integrity was assessed using standard denaturing agarose gel electrophoresis. Total RNA of each sample was used for labeling and array hybridization. Array scanning using the Agilent Scanner G250C. Scanned images were then imported into NimbleScan software (version 2.5) for expression data analysis. Differentially expressed LncRNAs were filtered out for further study.
2013-09-26 | E-GEOD-51146 | biostudies-arrayexpress
Project description:Proteogenomic anlalysis of glioblastoma (GBM)
| PRJNA627121 | ENA
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
Project description:Characterization of gene expression for a panel of 50 in vitro and in vivo models of glioblastoma (GBM). Models include subcutaneously established xenograft lines, orthotopically grown subcutaneously established xenograft lines, serum derived cell lines and stem cell media derived cell lines. Multiple replicates of each line were run on different dates to determine the effect of batch and processing date on reproducibility of gene expression profiles 117 samples analyzed from 50 distinct GBM xenografts or cell lines. Biological replicates from the same passage number were included for many, but not all, of the lines.
2011-12-01 | E-GEOD-26344 | biostudies-arrayexpress