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

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 array CGH copy number data obtained for five GBMs. We used estimated copy number to normalize sequencing-based methylation data.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49808 | GEO | 2013/08/13

SECONDARY ACCESSION(S): PRJNA214974

REPOSITORIES: GEO

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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)

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

2013-08-13 | GSE49412 | GEO

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

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

| S-ECPF-GEOD-49412 | biostudies-other

Prevalence of Copy-number neutral LOH in glioblastomas revealed by analysis of laser-microdissected tissues

Project description:We have employed a laser capture microdissection technique and single nucleotide polymorphism arrays to characterize genomic alterations associated with the development of glioblastomas. Combined analysis of LOH and copy number revealed that more than half of the identified 254 LOH loci showed no copy number alteration, indicating the presence of copy-number neutral LOH Keywords: DNA copy number, Loss of heterozygosity Affymetrix 50K SNP mapping arrays were used to profile 14 primary glioblastomas (GBMs) with matched blood DNA samples. Loss of heterozygosity (LOH) and copy number abnormality (CNA) profiles were derived from each tumour-blood pair.

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Prevalence of Copy-number neutral LOH in glioblastomas revealed by analysis of laser-microdissected tissues

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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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Longitudinal epigenome analysis of IDH-wildtype glioblastomas from initial and recurrent surgical specimens

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2024-11-19 | GSE279073 | GEO

Methylation data from glioblastoma tumor samples

Project description:Glioblastoma (GBM) is an incurable brain tumor carrying a dismal prognosis, which displays considerable heterogeneity. We have recently identified recurrent H3F3A mutations affecting two critical positions of histone H3.3 (K27, G34) in one-third of pediatric GBM. Here we show that each of these H3F3A mutations defines an epigenetic subgroup of GBM with a distinct global methylation pattern, and are mutually exclusive with IDH1 mutations (characterizing a CpG-Island Methylator Phenotype (CIMP) subgroup). Three further epigenetic subgroups were enriched for hallmark genetic events of adult GBM (EGFR amplification, CDKN2A/B deletion) and/or known transcriptomic signatures. We also demonstrate that the two H3F3A mutations give rise to GBMs in separate anatomic compartments, with differential regulation of OLIG1/2 and FOXG1, possibly reflecting different cellular origins. We identified six epigenetic and biological GBM subgroups displaying distinct global DNA methylation patterns, which harbor unique hotspot mutations, DNA copy-number alterations, and transcriptomic patterns. We investigated a subset of childhood (n=59) and adult GBMs (n=77) using the Illumina 450k methylation array. Six non-neoplastic brain tissue samples are included as controls.

2012-10-16 | E-GEOD-36278 | biostudies-arrayexpress

Patient specific orthotopic glioblastoma xenograft models recapitulate the histopathology and biology of human glioblastomas in situ (CGH)

Project description:Frequent discrepancies between preclinical and clinical results of anti-cancer agents demand a reliable translational platform that can precisely recapitulate the biology of human cancers. Another critical unmet need is the ability to predict therapeutic responses for individual patients. Toward this goal, we have established a library of orthotopic glioblastoma (GBM) xenograft models using surgical samples of GBM patients. These patient-specific GBM xenograft tumors recapitulate histopathological properties and maintain genomic characteristics of parental GBMs in situ. Furthermore, in vivo irradiation, chemotherapy, and targeted therapy of these xenograft tumors mimic the treatment response of parental GBMs. We also found that establishment of orthotopic xenograft models portends poor prognosis of GBM patients and identified the gene signatures and pathways signatures associated with the clinical aggressiveness of GBMs. Together, the patient-specific orthotopic GBM xenograft library represent the preclinically and clinically valuable “patient tumor’s phenocopy” that represents molecular and functional heterogeneity of GBMs.

2013-01-18 | GSE42577 | GEO

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