Similar Datasets
Project description:Samples were obtained from 52 non-recurrent GBM patients treated at Severance Hospital
2019-05-29 | GSE131837 | GEO
Project description:Gene expression profiles of non-recurrent human glioblastoma tumorspheres
| PRJNA667330 | ENA
Project description:Glioblastoma (GBM) bears a dismal prognosis with rapid relapse following complete resection and radiochemotherapy. The involvement of microRNAs in tumor progression has been demonstrated in hepatoma, breast cancer, and prostate cancers. However, the microRNAs involved in modulating the progression and relapse of GBM are still unclear. Initially, we compared the miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases. miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases.
2014-09-28 | E-GEOD-32466 | biostudies-arrayexpress
Project description:Recurrent glioblastoma (GBM) has a grim prognosis, though MGMT promoter methylation and IDH mutation provide a significant survival advantage. The product of IDH mutation, 2-hydroxyglutarate, increases global DNA methylation by inhibiting demethylases. While lower-grade IDH-mutant gliomas demonstrate increased methylation as a result of this process, DNA becomes relatively hypomethylated during progression from low-grade glioma to secondary (IDH-mutant) GBM. Here we show that global DNA hypomethylation also occurs during primary (IDH-wild type) GBM recurrence. Moreover, in a phase I trial of 14 patients with recurrent (IDH-wild type) GBM, we targeted DNA hypomethylation using a methyl donor treatment. In autopsied tumors from patients treated, we observed a global increase in DNA methylation compared to initial tumor. These results suggest that hypomethylation is a marker for recurrence, and its reprogramming represents a potential therapeutic vulnerability.
2021-12-31 | GSE111627 | GEO
Project description:Glioblastoma multiforme (GBM) is the most lethal brain malignant neoplasm, associated with poor prognosis and high recurrence. The mechanisms involved in GBM development and recurrent remains largely unknown. Hence, it’s considerably imperative to explore the potential targets and unravel the mechanism implicated in GBM tumorigenesis and recurrence. In our study, mass spectrometry-based label-free quantitative proteomics was employed to explore the proteomic profiling in non-paired samples of primary and recurrent GBM. Bioinformatic analysis of differentially expression proteins (DEPs) were applied to screen the hub genes. Subsequently, hub genes expression was verified by western blot and immunohistochemistry (IHC) in GBM tissues, followed by its biological effect on GBM at a cellular level determined. We contoured the divergent landscape of proteome between primary and recurrent GBM, with only ten overlapped DEPs included. The several hub genes screened (e.g., CKAP4 and CANX) and enriched pathways correlated with primary GBM such as post-translation, metabolism, energy pathways and cell growth were profiled. Furthermore, CKAP4 was implicated in proliferation, migration and invasion of A172 and T98G cell lines. However, UQCRC1, together with relative enriched pathways such as oxidative phosphorylation, were screened in recurrent GBM. Establishment of the proteomics and several candidate proteins identified could pose considerable access to understand complex biochemical processes and obtain a better picture of GBM biology.
2021-06-06 | PXD026503 |
Project description:Circular RNAs are single-stranded covalently closed non-coding RNAs expressed in a variety of tissues and cells. Glioblastoma (GBM) is the most aggressive and lethal tumor in the central nervous system, characterized by high recurrence and mortality rates. Here we explore circRNA expression profiles in 26 primary and 3 recurrent GBM samples and compare them to healthy brain tissue. Additionally we compare expression of circRNA in GBM patients blood in comparison to healthy donor blood.
2024-06-29 | GSE196695 | 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.
2020-11-17 | PXD017952 | Pride
Project description:Glioblastoma multiforme (GBM) is the most aggressive and frequent primary brain tumor with dismal prognosis which might be due to the resistance to the current standard chemotherapeutic regimens and high recurrence rate even after total resection of GBM mass. Here, to gain the mechanistic insights on the altered phenotypic acquisition of recurrent tumors compared to the corresponding primary tumors, we performed gene expression profiling on the 43 cases of GBM tumors including 15 paired recurrent and primary GBMs. Unsupervised and consensus clustering analyses revealed two subtypes of G1 and G2, which were enriched with proliferation, and neuron-like gene expression traits, respectively. Most of the primary tumors were classified into G1, while the recurrent tumors were classified into both G1 and G2 groups. The gene expression of recurrent GBMs in G2 group have changed from proliferation type to neuron-like type, while the other recurrent GBMs in the G1 group showed no significant subtype change. In addition, we observed that the recurrent tumors in G1 subtype were characterized with the expression of stemness-related genes and DNA-repair genes. Of the G1 subtype classifier genes, AURKA/B and HOX genes were identified as key hub regulators. On the other hand, the recurrent G2 tumors have acquired the expression of MGMT but suppression of MSH6 gene, which may lead to TMZ resistance. The consistency of these findings could be validated with independent data sets. In summary, our molecular classification of recurrent GBMs could suggest that the differential mechanisms of drug resistance be involved in the tumor recurrence. Targeting the subtype-specific mechanisms might be a beneficial strategy for the treatment of recurrent GBMs.
2015-10-20 | GSE62153 | GEO
Project description:Glioblastoma (GBM) bears a dismal prognosis with rapid relapse following complete resection and radiochemotherapy. The involvement of microRNAs in tumor progression has been demonstrated in hepatoma, breast cancer, and prostate cancers. However, the microRNAs involved in modulating the progression and relapse of GBM are still unclear. Initially, we compared the miRNA expression profiles between primary and recurrent GBM tissues from the same patient in twelve independent cases.
2014-09-28 | GSE32466 | GEO
Project description:Gene expression profiles of non-recurrent human glioblastoma tissues
| PRJNA545098 | ENA