Transcriptomic analysis of pre- and post-treatment GBM tumors (GBM-28 vs. GBM-37)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE158772 | GEO | 2025/05/31
REPOSITORIES: GEO
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Project description:Transcriptomic analysis of pre- and post-treatment GBM tumors (GBM-28 vs. GBM-37)
| PRJNA666454 | ENA
Project description:Glioblastoma multiforme (GBM) is a highly aggressive primary brain cancer with significant transcriptomic heterogeneity among patients. Our study aims to contribute to the field of personalized medicine for GBM patients by providing comprehensive transcriptomic profiles of GBM patients (N = 45) who underwent concurrent chemoradiotherapy with temozolomide at Seoul National University Hospital. Additionally, we include transcriptomic profiles of normal brain tissue obtained from GBM patients. This dataset may add depth to existing knowledge by uncovering distinct transcriptomic signatures related to aggressiveness in GBM, and may inform future research on the molecular mechanisms underlying transcriptomic features of GBM and personalized treatment strategies.
2024-04-14 | GSE263588 | GEO
Project description:Glioblastoma (GBM) is among the most aggressive cancers. Despite aggressive radiotherapy and treatment with the alkylating agent temozolomide (TMZ), patients ultimately succumb to the disease. Although much interest has focused on highly tumorigenic GBM stem cells (GSCs), adaption of a concept from microbial research proposes that a minor population of dormant âpersisterâ cells in cancer evade current therapies. To separate dormant and treatment-resistant tumor cells in human GBM tumorspheres, we have refined density gradient protocols previously used for separation of neurosphere-forming neural stem cells (NSCs). We find that a minor cell population in human GBM tumorsphere cultures and patient-derived tumor biopsies display increased cell density. These high-density GBM cells (HDGCs) display dormancy, variable expression of proposed GSC markers, and 10-100 fold higher levels of reprogramming gene expression compared to low-density GBM cells (LDGCs). Transcriptional profiling data confirmed the slow-cycling state of HDGCs. As a result, HDGCs show decreased tumorsphere formation capacity in vitro and reduced tumorigenicity in vivo. Using tumorspheres and xenografts, we demonstrated that HDGCs show increased treatment-resistance to ionizing radiation (IR) and temozolomide treatment compared to LDGCs. Similar to the NSC lineage, our data suggest that dormant HDGCs become increasingly sensitive to anti-proliferative therapies as they become activated and further differentiate. In conclusion, density gradients represents a marker-independent approach to separate dormant and treatment-resistant tumor cells in human GBMs and other solid cancers. 12 samples, no replicates, derived from 5 individual patients
2016-07-01 | E-GEOD-71116 | biostudies-arrayexpress
Project description:We analyzed, by HTA 2.0, the GBM cell lines LN-18, LN-229, and U-87 MG after fluoresence-activated cell sorting (FACS) into ABCB5+ and ABCB5- fractions. Poor prognosis associated with glioblastoma multiforme (GBM) results from tumor resistance to therapy and high rate of recurrence. Compelling evidence suggests this is driven by subpopulations of slow-proliferating cancer stem cells with tumor-initiating potential. ATP-binding cassette member B5 (ABCB5) has been identified as a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in diverse human malignancies. In the current study, we examined the potential role of ABCB5 in growth and chemoresistance of GBM. We found ABCB5 to be preferentially expressed in clinical GBM tumors and co-expressed with the stem cell marker CD133 in subpopulations of human GBM cell lines U-87 MG, LN-18 and LN-229. Antibody-mediated functional ABCB5 blockade inhibited proliferation and survival of human GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis. Likewise, in an in vivo GBM xenograft study in immunodeficient mice, anti-ABCB5 monoclonal antibody treatment inhibited tumor growth and sensitized tumors to TMZ therapy. Mechanistically, we demonstrated that ABCB5 regulates cell cycle checkpoint molecules to revoke drug-induced G2-M arrest and augments drug-mediated cell death. Overall, our data establish ABCB5 as a marker of GBM chemoresistance and point to the potential of ABCB5 targeting in improvement of current GBM therapies.
2020-03-05 | GSE127895 | GEO
Project description:Glioblastoma multiforme(GBM) is the most common and lethal malignant primary brain tumor. Temozolomide (TMZ) is a promising chemo-therapeutic agent to treat GBM. However, resistance to TMZ develops quickly with a high frequency. The mechanisms underlying GBM cells’ resistance to TMZ are not fully understood. Non-coding RNAs are aberrantly expressed in many cancers and are highly involved in their pathogenesis including drug-resistence. In order to systematically study the role of miRNAs in GBM cells' resistence to TMZ , we built gene expression profiles of TMZ-resistant cell line and TMZ-sensitive cell line using miRNA gene expression microarrays.
2020-07-04 | GSE100775 | GEO
Project description:Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. The purpose of the present study was to identify GBM cell-selective secreted proteins by analyzing conditioned media (CM) from GBM, breast, and colon cancer cell lines using sequential window acquisition of all theoretical spectra mass spectrometry (SWATH-MS) and targeted proteomics. We identified 26,041 peptides derived from 2,371 proteins in the CM from GBM and the other cancer cell lines. Among the proteins identified, 15 showed significantly higher expression in the CM from GBM cell lines than in those from other cancer cell lines.
2020-09-19 | PXD016898 | JPOST Repository
Project description:Comparing the transcriptomic profiles of GBM-37 cells treated with control and NUPR1 v.1 siRNA. Goal was to examine the effects of NUPR1 v.1 on malignant mesenchymal transformation of GBM tumor after conventional treatment
2025-05-31 | GSE158774 | GEO
Project description:Glioblastoma (GBM) is among the most aggressive cancers. Despite aggressive radiotherapy and treatment with the alkylating agent temozolomide (TMZ), patients ultimately succumb to the disease. Although much interest has focused on highly tumorigenic GBM stem cells (GSCs), adaption of a concept from microbial research proposes that a minor population of dormant “persister” cells in cancer evade current therapies. To separate dormant and treatment-resistant tumor cells in human GBM tumorspheres, we have refined density gradient protocols previously used for separation of neurosphere-forming neural stem cells (NSCs). We find that a minor cell population in human GBM tumorsphere cultures and patient-derived tumor biopsies display increased cell density. These high-density GBM cells (HDGCs) display dormancy, variable expression of proposed GSC markers, and 10-100 fold higher levels of reprogramming gene expression compared to low-density GBM cells (LDGCs). Transcriptional profiling data confirmed the slow-cycling state of HDGCs. As a result, HDGCs show decreased tumorsphere formation capacity in vitro and reduced tumorigenicity in vivo. Using tumorspheres and xenografts, we demonstrated that HDGCs show increased treatment-resistance to ionizing radiation (IR) and temozolomide treatment compared to LDGCs. Similar to the NSC lineage, our data suggest that dormant HDGCs become increasingly sensitive to anti-proliferative therapies as they become activated and further differentiate. In conclusion, density gradients represents a marker-independent approach to separate dormant and treatment-resistant tumor cells in human GBMs and other solid cancers.
2016-07-01 | GSE71116 | GEO
Project description:GBM is a heterogenous brain tumor with hyperproliferation of endothelial cells. In order to understand the cellular mechanism of vasculogenesis in GBM, four fractions of cells are seperated. Microarray assays was performed to examine the potential lineage relationship and the signal pathways involved in determining the cell identity and function. Four subpopulation of cells were seperated from two independent GBM dissociates by FCAS assay based on the expression of membrane marker CD133 and CD144. Total RNA was extracted from freshly sorted cells without any culture.
2010-11-21 | E-GEOD-24244 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) is the most aggressive form of brain tumors. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to such treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and -5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased of cell proliferation, and increased cell cycle arrest and apoptosis in comparison to only irradiated cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation and cell cycle regulation. To our knowledge, this is the first study to describe role of miR-338-5p in GBM and its potential to improve sensitivity of GBM to radiation. Study was performed on three glioblastoma multiforme cell lines A172, T98G and U87MG. This experiment was performed on Affymetrix GeneChip Human Gene ST 1.0 to elucidate the targets of miRNA-338-5p. Cell lines were seeded 24 hours prior transfection. After transfection with pre-miR338-5p or negative control cell were cultured for 24 hours and harvested. RNA was isolated using MirVana miRNA Isolation Kit (Ambion, USA) and checked for RNA integrity by Bioanalyzer 2100 and purity by ratios 260/280>1.8 and 260/230>1.8 by Nanodrop2000.
2015-12-10 | E-GEOD-75789 | biostudies-arrayexpress