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Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

ABSTRACT: PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE55061 | GEO | 2014/06/02

SECONDARY ACCESSION(S): PRJNA238357

REPOSITORIES: GEO

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Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

Project description:PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells. Neonatal mice were injected with RCAS PDGFB GFP. At symptoms, or at 12 weeks post injection, GFP+DAPI- tumor cells were sorted for RNA extraction and hybridization on Affymetrix microarrays. The mouse strain used was a mixed background of C57/BL6 and FVB/N. Ptprd mice were from Uetani et al. 2000 and p16/Nestin-tvA mice were from Tchouganouva et al. 2007.

2014-06-02 | E-GEOD-55061 | biostudies-arrayexpress

Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB driven gliomas

Project description:Here we describe the use of a high-throughput pipeline coupled to the commonly used tissue-specific retroviral RCAS-TVA mouse tumor model system. Utilizing next generation sequencing, we show that retroviral integration sites can be reproducibly detected in malignant stem cell lines generated from RCAS-PDGFB-driven glioma biopsies.

2022-07-05 | GSE207264 | GEO

Mus musculus

Project description:Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

| PRJNA238357 | ENA

Effects of the Combination Therapy of a CDK4/6 and a MEK inhibitor in a Mouse Model of Diffuse Midline Glioma

Project description:Diffuse intrinsic pontine glioma (DIPG) arises in the brainstem of children, leading tumor-related death among children. A heterozygous histone H3.3K27M mutation has been shown to occur in ~80% of DIPGs, and results in brainstem gliomagenesis. There is no clinical trial for the patients with DIPG that proved to prolong survival time so far. Recently, CDK4/6 inhibitor showed feasibility and early therapeutic effect against DIPG. Also, recent research with human DIPG specimens have detected the MAPK pathway highly activated. Here, we evaluated a novel combination therapy with CDK4/6 inhibitor and MEK inhibitor to the mouse DIPG model. In order to generate DIPG‐bearing mice, we are using the RCAS/Tv‐a system, with which we are able to target specific genetic alterations in RCAS viruses (avian retroviruses) to specific cells‐of‐origin using transgenic Tv‐a‐expressing mice (Tv‐a being the receptor for RCAS viruses). We injected P3‐P5 Nestin-Tv-a;p53fl/fl mice (C56Bl/6 background) with RCAS‐PDGF‐A + RCAS‐H3.3K27M, and RCAS-Cre. The mice are treated with vehicle (methylcellurose), ribociclib as monotherapy, trametinib as monotherapy, and ribociclib and combination as combination. For short-term use, tumor tissues treated with ribociclib showed cytostatic effect, and those treated with trametinib showed cytotoxic effect, and those with combination showed both. Long-term use showed that combination therapy modestly prolonged mice survival compared with vehicle. Therefore, we need to find how DIPG showed registence to the long-term chemotherapy.

2021-09-28 | GSE184786 | GEO

RNAseq analysis of murine brainstem gliomas with and without H3.3K27M

Project description:Using the RCAS/tv-a system, we induced murine brainstem gliomas (PDGF-B; p53 loss using RCAS-Cre with and without H3.3K27M) in Nestin tv-a; p53 floxed mice

2017-05-11 | GSE98765 | GEO

Candidatus Portiera aleyrodidarum TV strain:TV

Project description:Candidatus Portiera aleyrodidarum TV strain:TV Genome sequencing

| PRJNA190632 | ENA

Transcription profiling of human 293 cells infected with either RCAS-beta-catenin S37A or RCAS-GFP

Project description:293 cells, infected with RCAS-beta-cateninS37A or RCAS-GFP

2007-08-04 | E-GEOD-1473 | biostudies-arrayexpress

Novel genetically engineered H3.3G34R model reveals cooperation with ATRX loss in upregulation of PRC2 targets, NOTCH activation, promotion of neuronal lineage

Project description:Pediatric high-grade gliomas (pHGGs) are an aggressive pediatric CNS tumor, often characterized by mutations in H3F3A, the gene that encodes Histone H3.3 (H3.3). Substitution of the Glycine at position 34 of H3.3 with either Arginine or Valine (H3.3G34R/V), was recently described and characterized in a large cohort of pHGG samples as occurring in 5-20% of pHGGs. We developed a genetically engineered mouse model (GEMM) that incorporates PDGF-A activation, TP53 loss and the H3.3G34R mutation both in the presence and loss of Alpha thalassemia/mental retardation syndrome X-linked (ATRX), which is commonly mutated in H3.3G34 mutant pHGGs. Nestin Tv-a; p53 fl/fl and Nestin Tv-a; p53 fl/fl; ATRX fl/fl mice were injected with DF-1 cells transfected with RCAS-Cre, RCAS-PDGFA, and either RCAS-H3.3WT-GFP or RCAS-H3.3G34R-GFP. By 210 days old, a majority of mice develop symptoms of tumor growth (erratic behavior, domed head, ataxia) or have 20% weight loss and are euthanized. Our goal is to develop a biologically relevant animal model of pHGG in order to probe the downstream effects of the H3.3G34R mutation in the context of vital co-occurring mutations.

2023-03-04 | GSE197988 | GEO

Effect of ATRX deficiency on gene expression of RCAS-nTva derived murine gliomas [RNA-seq: ATRX_Immuno_Tumor]

Project description:To investigate the impact of ATRX loss on tumor microenvironment we generated ATRX-intact and -deficient tumors in immune competent mice with the RCA-nTva system. Mice were injected with a tumorigenic RCAS construct (PDGFa and shTP53) and an RCAS bearing CRE recombinase. This was performed in mice that were ATRX wt and ATRX floxed.

2023-05-08 | GSE231831 | GEO

Effect of ATRX deficiency on gene expression of RCAS-nTva derived murine gliomas [RNA-seq: ATRX_Immuno_cell_line]

2023-05-08 | GSE231830 | GEO

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