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Expression data from five primary human glioblastomas (frozen surgical resection) and one non-neoplastic adult brain (frozen autopsy tissue)

ABSTRACT: DNA hypomethylation could lead to activation of alternate promoters in GBM. We profiled DNA methylation and H3K4me3 genome-wide, and also performed expression and copy number analysis on the same samples In this dataset, we include all expression data obtained for five GBMs and one normal brain. We identified loci with concurrent DNA hypomethylation and H3K4me3 in GBM, and analyzed expression of the nearest gene in the same sample using these data

ORGANISM(S): Homo sapiens

PROVIDER: GSE49412 | GEO | 2013/08/13

SECONDARY ACCESSION(S): PRJNA214968

REPOSITORIES: GEO

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Expression data from five primary human glioblastomas (frozen surgical resection) and one non-neoplastic adult brain (frozen autopsy tissue)

Project description:DNA hypomethylation could lead to activation of alternate promoters in GBM. We profiled DNA methylation and H3K4me3 genome-wide, and also performed expression and copy number analysis on the same samples In this dataset, we include all expression data obtained for five GBMs and one normal brain. We identified loci with concurrent DNA hypomethylation and H3K4me3 in GBM, and analyzed expression of the nearest gene in the same sample using these data Six total samples were analyzed. Each GBM sample was compared to normal brain to obtain expression changes

2013-08-13 | E-GEOD-49412 | biostudies-arrayexpress

Copy number data from five primary human glioblastomas (frozen surgical resection)

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Copy number data from five primary human glioblastomas (frozen surgical resection)

Project description:DNA hypomethylation could lead to activation of alternate promoters in GBM. We profiled DNA methylation and H3K4me3 genome-wide, and also performed expression and copy number analysis on the same samples In this dataset, we include all array CGH copy number data obtained for five GBMs. We used estimated copy number to normalize sequencing-based methylation data. Five total samples were analyzed.

2013-08-13 | E-GEOD-49808 | biostudies-arrayexpress

Expression data from five primary human glioblastomas (frozen surgical resection) and one non-neoplastic adult brain (frozen autopsy tissue)

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Project description:We aimed to identify a clinically useful biomarker using DNA methylation-based information to optimize the management of glioblastoma (GBM) patients. We identified a novel six-CpGs signature that predicts the clinical outcome in GBM. The methylation profiling of 79 GBM patients has been used as a validation cohort to demonstrate the performance and the robustness of the identified six-CpGs signature. The status of the âMGMTâ biomarker, traditionally used by clinicians to predict survival in GBM, is also indicated per sample.

2017-12-15 | E-MTAB-4969 | biostudies-arrayexpress

DNA methylome evolution and reprogramming in recurrent glioblastoma

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.

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Surgical resection of glioblastomas induces pleiotrophin-mediated self-renewal of glioblastoma stem cells in recurrent tumors.

Project description:BackgroundGlioblastomas are highly resistant to therapy, and virtually all patients experience tumor recurrence after standard-of-care treatment. Surgical tumor resection is a cornerstone in glioblastoma therapy, but its impact on cellular phenotypes in the local postsurgical microenvironment has yet to be fully elucidated.MethodsWe developed a preclinical orthotopic xenograft tumor resection model in rats with integrated 18F-FET PET/CT imaging. Primary and recurrent tumors were subject to bulk and single-cell RNA sequencing. Differentially expressed genes and pathways were investigated and validated using tissue specimens from the xenograft model, 23 patients with matched primary/recurrent tumors, and a cohort including 190 glioblastoma patients. Functional investigations were performed in vitro with multiple patient-derived cell cultures.ResultsTumor resection induced microglia/macrophage infiltration, angiogenesis as well as proliferation and upregulation of several stem cell-related genes in recurrent tumor cells. Expression changes of selected genes SOX2, POU3F2, OLIG2, and NOTCH1 were validated at the protein level in xenografts and early recurrent patient tumors. Single-cell transcriptomics revealed the presence of distinct phenotypic cell clusters in recurrent tumors which deviated from clusters found in primary tumors. Recurrent tumors expressed elevated levels of pleiotrophin (PTN), secreted by both tumor cells and tumor-associated microglia/macrophages. Mechanistically, PTN could induce tumor cell proliferation, self-renewal, and the stem cell program. In glioblastoma patients, high PTN expression was associated with poor overall survival and identified as an independent prognostic factor.ConclusionSurgical tumor resection is an iatrogenic driver of PTN-mediated self-renewal in glioblastoma tumor cells that promotes therapeutic resistance and tumor recurrence.

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