Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cross-species genomics identifies postanatal CPE as novel choroid plexus carcinoma oncogenes.

ABSTRACT: Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs [GSE60892; GSE60899], we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy.

ORGANISM(S): Mus musculus

PROVIDER: GSE61659 | GEO | 2015/05/01

SECONDARY ACCESSION(S): PRJNA261821

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cross-species genomics identifies postanatal CPE as novel choroid plexus carcinoma oncogenes.

Project description:Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs [GSE60892; GSE60899], we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy. CPC mouse model samples of tumors derived from choroid plexus epithelium (CPE) cells that are Tp53/RB/Pten null in FVB mice. Female CD1 nude (host) mice were transfected with postanatal CPE and compared with a medulloblastoma normal mouse embryonic, postnatal and adult controls (loxP TP53/RB/PTEN (no Cre)) Implanted and reimplanted are from the orthotropic transplants of the primary tumor or later tumors

2015-05-01 | E-GEOD-61659 | biostudies-arrayexpress

Cross-species genomics identifies TAF12, NFYC and RAD54L as novel choroid plexus carcinoma oncogenes

| EGAS00001000961 | EGA

Myc and loss of p53 cooperate to drive formation of choroid plexus carcinoma

Project description:Choroid plexus carcinoma (CPC) is a rare brain tumor that occurs most commonly in very young children, and has a dismal prognosis despite intensive therapy. Improved outcomes for CPC patients depend on a deeper understanding of the mechanisms underlying the disease. We developed transgenic models of CPCs by activating the Myc oncogene and deleting the Trp53 tumor suppressor gene in murine neural stem cells or progenitors. Murine CPCs resemble their human counterparts at a histological level, and like the hypodiploid subset of human CPCs, exhibit multiple whole-chromosome losses, particularly of chromosomes 8, 12 and 19. Analysis of murine and human CPC gene expression profiles and copy number changes reveals altered expression of genes involved in cell cycle, DNA damage response and cilium function. Finally, high throughput drug screening identifies small molecule inhibitors that decrease the viability of CPCs. These models will be valuable tools for understanding the biology of choroid plexus tumors and for testing novel approaches to therapy.

2020-01-28 | GSE126408 | GEO

Comparative Computational RNA Analysis of Cardiac-Derived Progenitor Cells and Their Extracellular Vesicles

Project description:We aimed to examine differences between c-kit+ progenitor cells (CPCs) and CPC-derived extracellular vesicles (EV) RNA content. We isolated CPCs from cardiac biopsies of patients with congenital heart disease using magnetic bead sorting. We expanded CPCs, reduced serum for 24hrs, and collected secreted EVs from conditioned media with sequential ultracentrifugation. We isolate RNA from CPCs and CPC-EVs and sequence total RNA and miRNA. Sequencing was performed in at two different facilities: "E" and "N".

2022-11-21 | GSE196556 | GEO

Comparative Computational RNA Analysis of Cardiac-Derived Progenitor Cells and Their Extracellular Vesicles [miRNA-seq]

2022-12-31 | GSE202347 | GEO

Comparative Computational RNA Analysis of Cardiac-Derived Progenitor Cells and Their Extracellular Vesicles [RNA-Seq]

2022-12-31 | GSE202345 | GEO

Dissecting the Molecular Relationship Between Cardiac And Bone Marrow-Derived Progenitor Cells

Project description:Baseline gene expression of mouse Cardiac Progenitor Cells (CPC) We used microarrays to analyze the global gene expression of mouse CPCs. Compare the gloable gene expression of mouse CPCs and Cardiomyocytes. Although the chip is two color, we only used Cy5 as the data channel.

2012-12-01 | E-GEOD-41175 | biostudies-arrayexpress

A Regulatory Pathway Involving Notch1/β-Catenin/Isl1 Determines Cardiac Progenitor Cell Fate

2009-05-13 | GSE15232 | GEO

A Regulatory Pathway Involving Notch1/β-Catenin/Isl1 Determines Cardiac Progenitor Cell Fate

Project description:The regulation of multipotent cardiac progenitor cell (CPC) expansion and subsequent differentiation into cardiomyocytes, smooth muscle, or endothelial cells is a fundamental aspect of basic cardiovascular biology and cardiac regenerative medicine. However, the mechanisms governing these decisions remain unclear. Here, we show that Wnt/β-Catenin signaling, which promotes expansion of CPCs, is negatively regulated by Notch1-mediated control of phosphorylated β-Catenin accumulation within CPCs, and that Notch1 activity in CPCs is required for their differentiation. Notch1 positively, and β-Catenin negatively, regulated expression of the cardiac transcription factors, Isl1, Myocd and Smyd1. Surprisingly, disruption of Isl1, normally expressed transiently in CPCs prior to their differentiation, resulted in expansion of CPCs in vivo and in an embryonic stem (ES) cell system. Furthermore, Isl1 was required for CPC differentiation into cardiomyocyte and smooth muscle cells, but not endothelial cells. These findings reveal a regulatory network controlling CPC expansion and cell fate that involve unanticipated functions of β-Catenin, Notch1 and Isl1 that may be leveraged for regenerative approaches involving CPCs. YFP+ cells marking precardiac mesoderm (Isl1-cre domain) were FACS-sorted (w/wo stabilized Beta-catenin). Their total RNA was amplified with the WT-Ovation Pico RNA Amplification System, fragmented and labeled with the FL-Ovation cDNA Biotin Module V2 (Nugen). The hybridization, staining and scanning of the Affymetrix GeneChips were performed in the Gladstone Genomics Core Lab. Raw data generated from at least three independent experiments were further analyzed by the group of Dr. Ru-Fang Yeh at the Center for Informatics and Molecular Biostatistics, UCSF.

2009-05-13 | E-GEOD-15232 | biostudies-arrayexpress

Dissecting the Molecular Relationship Between Cardiac And Bone Marrow-Derived Progenitor Cells

Project description:Baseline gene expression of mouse Cardiac Progenitor Cells (CPC) We used microarrays to analyze the global gene expression of mouse CPCs.

2012-12-01 | GSE41175 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data