Affymetrix SNP array data for NF1-associated glioma risk
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE62215 | GEO | 2015/02/20
SECONDARY ACCESSION(S): PRJNA263489
REPOSITORIES: GEO
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Project description:We performed whole genome SNP profiling on DNA samples from 236 patients with NF1, 123 with glimoa tumors and 113 without; 117 females and 119 males, together with 29 control samples. To identify polymorphisms in human adenylate cyclase 8 (AC8) which correlate with glioma risk in NF1 in a sex-specific manner, Ac8 SNP were extracted and further analyzed for their sex-specific NF1-associated glioma risk. Three SNPs on ADCY8 were found signficant while other SNPs on CXCR7 and ADCYAP1 were promising. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from blood samples or saliva samples in three separate sets with one processed in Washington University and two in University of Utah. The data included 29 control samples and 236 NF1 patient samples (123 with and 113 without GBM) with 153 blood specimen and 97 saliva specimen.
2015-02-20 | E-GEOD-62215 | biostudies-arrayexpress
Project description:Affymetrix SNP array data for NF1-associated glioma risk
| PRJNA263489 | ENA
Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the expression changes of genes induced by inactivation of Tp53 and Nf1 can be a clue to clarify the mechanism of gliomagenesis. We examined the expressions of glioma in MADM mouse at post-natal 150 days (n=3) and of normal brain in Tp53 and Nf1 wild type mouse at post-natal 150 days (n=2). We used SurePrint G3 Mouse GE 8×60K array slides (G4858A, Agilent Technologies).
2017-06-30 | GSE91050 | GEO
Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the expression changes of genes induced by inactivation of Tp53, Nf1 and EZH2 can be a clue to clarify the mechanism of gliomagenesis. We examined the expressions of glioma cells in MADM mouse (n=2), EZH2 knocked-out MADM glioma tissues (n=3) and neural stem cell (NSC), astrocyte established with normal mice brains (n=2, respectively) and TP53 knocked-out astrocytes, derived from TP53 knocked-out mice (n=2). We used SurePrint G3 Mouse GE 8×60K array slides (G4858A, Agilent Technologies).
2020-02-20 | GSE110927 | GEO
Project description:A core task to understand the consequences of non-coding single nucleotide polymorphisms (SNP) is to identify their genotype specific binding of transcription factor (TF). Here, we generate a large-scale TF-SNP interaction map for a selection of 116 colorectal cancer (CRC) risk loci and validated TF binding to 10 putatively functional SNPs. Our data further revealed TF binding complexity adjacent to the 116 risk loci, adding an additional layer of understanding to regulatory networks associated with CRC relevant loci.
2017-02-23 | PXD004435 | Pride
Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the changes of histone modifications induced by inactivation of Tp53 and Nf1 can be a clue to clarify the mechanism of gliomagenesis. We examined the histone modifications of glioma in MADM mouse at post-natal 150 days (n=3) and post-natal 8 days (n=1) and NSC, astrocyte derived from normal mice brain (both n=1) ). We used customized SurePrint G3 Mouse GE 2×400K array slides (G4858A, Agilent Technologies).
2020-02-20 | GSE110926 | GEO
Project description:Solid cancers develop within a supportive microenvironment that promotes tumor formation and continued growth through the elaboration of mitogens and chemokines. Within these tumors, monocytes (macrophages and microglia) represent rich sources of these stromal factors. Leveraging a genetically-engineered mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumor (optic glioma), previous studies have demonstrated that microglia are important for glioma formation and maintenance. To identify the tumor-associated microglial factors that support glioma growth (gliomagens), we employed a comprehensive large scale discovery effort using optimized advanced RNA-sequencing methods. Candidate gliomagens were prioritized to identify potential secreted or membrane-bound proteins, which were next validated by quantitative RT-PCR and RNA FISH following minocycline-mediated microglial inactivation in vivo. Using these selection criteria, Ccl5 was identified as a highly expressed chemokine in both genetically engineered Nf1 mouse and human optic gliomas. As a candidate gliomagen, recombinant Ccl5 increased Nf1-deficient optic nerve astrocyte growth in vitro. Importantly, consistent with its critical role in maintaining tumor growth, Ccl5 inhibition with neutralizing antibodies reduced Nf1 mouse optic glioma growth in vivo. Collectively, these findings establish Ccl5 as critical stromal growth factor in low-grade glioma maintenance relevant to future microglia-targeted therapies for brain tumors.
2016-08-17 | GSE65831 | GEO
Project description:As the list of putative driver mutations in glioma grows, we are just beginning toAs the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous, glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma. Mouse Gene 1.0 ST Microarrays from Affimetryx were used for microarray analysis. For each experiment, total RNA was fluorescently labeled and hybridized. 3 cell lines derived from in vivo electroporated neural stem and progenitors were compared.
2015-05-28 | E-GEOD-69254 | biostudies-arrayexpress
Project description:Background: Signaling by receptor tyrosine kinases (RTK) is frequently dysregulated in gliomas. Inter-individual variability in the causes for dysregulated RTK signaling may have hampered the efficacy of targeted therapies. Using gene expression modules around key regulators in the RAS-RAF-MEK-MAPK cascade and in the phosphatidylinositol 3-kinase-AKT pathways, we developed a âRMPAâ clustering scheme to distinguish gliomas with varying extents of RTK signaling. Results: We identified gene modules consistently co-expressed with NF1 (NF1-M), Sprouty (SPRY-M) and PTEN (PTEN-M) in gliomas. Their signatures enabled robust clustering of adult diffuse gliomas of WHO grades II-IV into RMPAhigh and RMPAlow phenotypes in a morphology-independent manner. In five independent data sets from three continents containing more than 1500 adult diffuse gliomas, RMPAhigh gliomas were associated with poor prognosis while RMPAlow gliomas were not. The RMPAhigh and RMPAlow glioma subtypes showed distinct levels of the activities of RAS-RAF-MEK-MAPK cascade and PI3K-AKT pathway and harbored unique sets of genomic alterations in the RTK signaling-related genes. The RMPAhigh gliomas contained large numbers of immature vessel cells and tumor associated macrophages and both cell types expressed high levels of pro-angiogenic RTKs including MET, VEGFR1, KDR, EPHB4 and NRP1. Conclusion: Inter-glioma variability in RTK signaling activities can be defined using the RMPA clustering scheme. The combined signatures of NF1-M, SPRY-M and PTEN-M reflect RTK signaling activity both in the glioma cells and in the glioma microenvironment. Our data show that RTK signaling in the glioma microenvironment may play a pivotal role in glioma progression. Transcriptome data from 22 fresh gliomas (2 astrocytoma II, 1 oligodendrocytoma II, 7 oligoastrocytoma II, 4 anaplastic oligoastrocytoma III and 8 GBM) were obtained using Affymetrix Human Gene 1.0 ST Array. Unsupervised hierarchical clustering of the expression data for the SPRY-M, NF1-M and PTEN-M was performed on these transcriptome data to identify samples with RMPAhigh or RMPAlow signature.
2015-10-30 | E-GEOD-74462 | biostudies-arrayexpress
Project description:The study investigates the role of NF1 mutation and neuronal activity on the initiation of optic pathway glioma, a type of low-grade glioma. the RNAseq dataset investigates mRNA expression profile of human pilocytic astrocytomas (WHO grade I)
2021-03-30 | GSE163071 | GEO