Project description:Gene expression profiles generated from human tumor cells laser-microdissected from surgical samples of seven choroid plexus papillomas (Grade I WHO) as eight samples of epithelial cells lasermicrodissected from normal choroid plexus obtained at autopsy. Choroid plexus tumors are rare pediatric brain tumors derrived from the choroid plexus epithelium. Gene expression profiles of lasermicrodissected tumor cells from 7 individual choroid plexus tumor samples obtained at surgery were compared to gene expression profiles from non-neoplastic choroid plexus epithelial cells lasermicrodissected from normal non-neoplastic choroid plexus obtained at autopsy (Am J Surg Pathol. 2006 Jan;30(1):66-74.) in order to identfy genes differentially expressed in choroid plexus tumor cells.
Project description:We collected five DMG, five GBM (including two secondary GBM), and one peritumor samples from eleven patients requiring surgical resection. To establish an atlas for spatially-resolved gene expression, we performed short-read spatial transcriptomic sequencing on the tissue sections using the 10x Visium platform.
Project description:We performed scATAC-seq on glioblastoma tissue samples taken at time of initial surgical resection to map the global chromatin profiles of glioblastoma cells and associated non-neoplastic cells
Project description:MicroRNAs (miRNAs) are small (21-25 nucleotide in length) non-coding RNA molecules that negatively regulate protein expression. They are linked to cancer development and maintenance. In this work, studying gene expression profiles of 340 mammalian miRNAs with DNA microarrays, we selected 10 miRNAs gene features able to distinguish primary from secondary glioblastoma type; furthermore we verified that miR-21 and miR-155 up-regulatation seems to characterize the glioblastoma tumour state since it was found up-regulated in all samples analyzed compared to adult brain noneoplastic tissue. Since miR-21 function in glioblastoma cells was addressed previously we concentrated our efforts on miR-155 function. We found that miR-155 levels were markedly elevated both in primary and secondary glioblastomas tumours, in glioblastoma cell cultures and in 4 glioblastoma cell lines (U87, A172, LN229, and LN308) compared with adult brain tissue, CHP212-neuroblastoma cell lines and DAOY-1-medulloblastoma cell line. Since one of the miR-155 target was gamma-aminobutyric acid (GABA) A receptor (GABRA1) we verified if there was a relation between miR-155 up-regulation and GABRA1 expression. We demonstrated that, in cultured glioblastoma cells, knockdown of miR-155, which lower miR-155 expression to normal level, restore the normal expression of the gamma-aminobutyric acid (GABA) A receptor (GABRA1), making glioblastoma cells responsive to GABA cell cycle inhibiting signals. Our data suggest that aberrantly over-expressed miR-155 contribute to the malignant phenotype of the glioblastoma cells, promoting their unlimited growth. Keywords: miRNA expression profile We studied the expression profiles of 340 miRNAs in 97 glioblastoma tissues, of which 66 were primary glioblastomas and 27 were secondary glioblastomas. We have 66 replicates of primary glioblastoma and 27 replicates of secondary glioblastoma, each hybridized with the respective adult non-neoplastic brain tissue as a control.
Project description:Serial analysis of gene expression (SAGE) was used to get a global view of the gene profile in human hippocampus. A library were generated from control hippocampus, obtained by rapid autopsy. Keywords: hippocampus human inventory genes Control hippocampus (used to construct the SAGE control library) was obtained from a 48 years old man without history of seizures or other neurological diseases and no brain abnormalities at autopsy and histologically normal hippocampus. Autopsy was performed within 4 hours after death. Tissue was snap-frozen and stored at –80 0C until use. Total RNA was isolated from control hippocampus and hippocampal surgical specimens, using the Trizol method according to the manufacturer’s instructions (Invitrogen - Life Technologies, The Netherlands). Part of the anterior hippocampus of control (including sectors CA1- CA4 and dentate gyrus, DG) was used. Poly(A)+ RNA isolation, cDNA synthesis and all subsequent steps of the SAGE procedure were essentially performed as described (Velculescu et al., 1995) with minor modifications given previously (Michiels et al., 1999).
Project description:Epithelioid hemangioendothelioma (EHE) is a rare vascular sarcoma that is associated with a WWTR1-CAMTA1 fusion gene in greater than 90% of cases. We aimed to investigate the transcriptional pathways activated in EHE. Total RNA was isolated from EHE tumors from surgical resection or autopsy specimens (n=6) followed by RNA-Seq. The results of this study identified a unique transcriptional profile for EHE and helped to validate a novel murine model of EHE.
Project description:Gene expression profiling in 50 glial brain tumors and 4 normal brains using 42,000-feature cDNA microarrays (from total RNA). Tumors: 50 fresh-frozen glioma specimens subjected to standard WHO classification. Specimens included astrocytic [2 juvenile pilocytic astrocytomas, 1 low-grade astrocytic glioma, 1 anaplastic astrocytomas, 31 glioblastomas (of these 2 secondary glioblastomas and 2 gliosarcomas)], oligodendroglial [5 oligodendrogliomas, 3 anaplastic oligodendrogliomas], and 6 anaplastic oligoastrocytomas tumors. One tumor had been classified as glioneuronal neoplasm. Normal brain was purchased from Stratagene. Stratagene Universal Common Reference was used as reference RNA. The results provide insights into molecular mechanisms and pathways associated with gliomagenesis.
Project description:Genome wide DNA methylation profiling of human normal and epileptic brain tissue. The Illumina Infinium 850K Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850.000 CpGs in formalin-fixed paraffin-embedded surgical brain samples. Samples included 316 cases diagnosed with malformations of cortical development (MCD), non-MCD epilepsy or no-epilepsy autopsy controls.