Ena-DATASET-BGI-10-03-2017-07:43:30:089-161 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001003218 | EGA |
REPOSITORIES: EGA
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Project description:There are 116 liver cancer cases in this study and belong to LICA-CN project
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Project description:Glioblastoma (GBM) is a lethal brain cancer composed of heterogeneous cellular populations including glioma stem cells (GSCs) and their progeny differentiated non-stem glioma cells (NSGCs). Although accumulating evidence points out the significance of GSCs for tumour initiation and propagation, the roles of NSGCs remain elusive. Here we demonstrate that, when patient-derived GSCs in GBM tumours undergo differentiation with diminished telomerase activity and shortened telomeres, they subsequently become senescent phenotype, thereby secreting angiogenesis-related proteins, including vascular endothelial growth factors. Interestingly, these secreted factors from senescent NSGCs promote proliferation of human umbilical vein endothelial cells and tumorigenic potentials of GSCs in immunocompromised mice. These experimental data are likely clinically-relevant, since immunohistochemistry of both patient tumours of GBM and the patient GSC-derived mouse xenografted tumours detected tumour cells that express a set of markers for the senescence phenotype. Collectively, our data suggest that the inter-cellular signals from senescent NSGCs promote GBM tumour angiogenesis thereby increasing malignant progression of GBM. We monitored gene expression profiling in GSC, differentiated NSGC (GSC at day7 after serum exposure), and senescent NSGC (GSC at day30 after serum exposure) of GBM146 and GBM157.
2015-10-24 | E-GEOD-74304 | biostudies-arrayexpress
Project description:Glioblastoma (GBM) is a lethal brain cancer composed of heterogeneous cellular populations including glioma stem cells (GSCs) and their progeny differentiated non-stem glioma cells (NSGCs). Although accumulating evidence points out the significance of GSCs for tumour initiation and propagation, the roles of NSGCs remain elusive. Here we demonstrate that, when patient-derived GSCs in GBM tumours undergo differentiation with diminished telomerase activity and shortened telomeres, they subsequently become senescent phenotype, thereby secreting angiogenesis-related proteins, including vascular endothelial growth factors. Interestingly, these secreted factors from senescent NSGCs promote proliferation of human umbilical vein endothelial cells and tumorigenic potentials of GSCs in immunocompromised mice. These experimental data are likely clinically-relevant, since immunohistochemistry of both patient tumours of GBM and the patient GSC-derived mouse xenografted tumours detected tumour cells that express a set of markers for the senescence phenotype. Collectively, our data suggest that the inter-cellular signals from senescent NSGCs promote GBM tumour angiogenesis thereby increasing malignant progression of GBM.
2015-10-24 | GSE74304 | GEO
Project description:Among acute myeloid leukemias (AML) with normal karyotype (CN-AML), NPM1 and CEBPA mutations define WHO provisional entities accounting for ~60% of cases, but the remaining ~40% remains poorly characterized. By whole exome-sequencing (WES) of one CN-AML patient lacking mutations in NPM1, CEBPA, FLT3, MLL-PTD and IDH1, we newly identified a clonal somatic mutation in BCOR (BCL6 co-repressor), a gene located in chromosome X. Further analyses showed that BCOR mutations occurred in 11/262 (4.2%) CN-AML cases and represented a substantial fraction (14/82, 17.1%) of CN-AML patients showing the same genetic background as the index patient subjected to WES. BCOR somatic mutations were: i) disruptive events similar to germline BCOR mutations causing the oculo-cranio-facial-dental (OCFD) genetic syndrome; ii) associated with markedly decreased BCOR mRNA levels, absence of full-length BCOR and absent or low expression of a truncated BCOR protein; iii) almost mutually exclusive with NPM1 mutations and frequently associated with DNMT3A and RUNX1 mutations, pointing to a cooperation between these events. Finally, BCOR mutations correlated with poor outcome among a cohort of 160 CN-AML patients (28% versus 66% overall survival at 2 yrs, P=0.024). Our results implicate for the first time BCOR in the pathogenesis of CN-AML without NPM1 mutations.
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Project description:High-density single nucleotide polymorphism (SNP) arrays were used to investigate genome-wide copy number (CN) alterations and loss of heterozygosity (LOH) in glioblastomas (GBM) patients; our aim focused on the identification and detailed characterization of the genetic alterations of the chromosomes altered in these tumors and the identification of subgroups of GBM with distinct cytogenetic patterns of alteration for the affected chromosomes potentially associated with the behavior of the disease. Overall, gains of chromosome 7, losses of chromosomes 9p and 10 were the most frequent chromosomal alterations. The 7p11.2 region was amplified in several cases. Based on CN alterations for chromosomes 7, 9 and 10, five different cytogenetic patterns with a significant impact on patient survival were identified; noteworthy, cases with EGFR amplification showed a better survival, specifically among patients older than 60 years. In addition, our results provide further evidence about the relevance of the EGFR, CDKN2A/B, MTAP genes, and other genes coded in chromosome 10 in the pathogenesis of GBM. Altogether, our results confirm the cytogenetic heterogeneity of GBM and suggest that stratification of these tumors into genetic subsets based on the combined assessment of cytogenetic alterations involving chromosomes 7, 9 and 10, may contribute to the prognostic evaluation of GBM.
2012-11-30 | GSE42631 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE24446: Genetic abnormalities in GBM brain tumors GSE24452: Genetic abnormalities in various cell subpopulations of GBM brain tumors GSE24557: Exon-level expression profiles of GBM brain tumors Refer to individual Series
2010-11-21 | E-GEOD-24558 | biostudies-arrayexpress
Project description:In this study, we evaluated the effects of milli-meter waves on structured Glioblastoma organoids to assess the possibility of therapeutic applications. The exposure setup was completely developed, and the dosimetry carried on based on both numerical and experimental activities. Our results showed that continuous milli-meter waves at 30.5 GHz affect cell proliferation and apoptosis, thus not affecting the differentiation status of the organoids composing of GBM cells. By applying the power level of 0.1 W (RMS), we obtain a synergistic effect with the chemotherapeutic Temozolomide in terms of GBM cell death. All these data open the way to an interventional window in which to treat GBM cells (i.e. with TMZ) exploiting 30.5 GHz CW exposure for potential therapeutic purposes thus improving GBM future management, which remain extremely difficult so far. Our investigation sheds light on the characterization of possible bio-effects of MMW (30.5 GHz CW) on GBM organoids highlighting cell and molecular responses in a relevant 3D tumor model.
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