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Expression analysis of MADM based glioma mouse model and normal brain

ABSTRACT: 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).

ORGANISM(S): Mus musculus

PROVIDER: GSE110927 | GEO | 2020/02/20

REPOSITORIES: GEO

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Expression analysis of MADM based glioma mouse model

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

ChIP analysis of MADM based glioma mouse model

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).

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ChIP analysis of MADM based glioma mouse model

Project description:ChIP analysis of MADM based glioma mouse model

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Expression analysis of MADM based glioma mouse model and normal brain

Project description:Expression analysis of MADM based glioma mouse model and normal brain

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Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

2015-02-04 | GSE60660 | GEO

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Project description:Expression analysis of MADM based glioma mouse model

| PRJNA356744 | ENA

Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

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RNA-sequencing of tumor-associated microglia reveals Ccl5 as a stromal chemokine critical for neurofibromatosis-1 glioma growth

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

RNA-seq of mouse glioma tumors with or without ASCL1

Project description:Tamoxifen was administered to Glast-CreER;Nf1-flox/flox;Tp53-flox/flox or Glast-CreER;Ascl1-flox/flox;Nf1-flox/flox;Tp53-flox/flox at E14.5 to induce tumors in the brain

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