Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatocyte-specific knockout of Pten and of Pten and Tgfbr2 in mice

ABSTRACT: Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE66717 | GEO | 2016/02/26

SECONDARY ACCESSION(S): PRJNA277773

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Hepatocyte-specific knockout of Pten and of Pten and Tgfbr2 in mice

Project description:Gene expression of hepatocyt-specific knockout of Pten and of Pten and Tgfbr2 in mice as a model for human cholangiocarcinoma was determined Affymetrix Mouse 1.0ST chips were used to measure gene expression Gene expression of the following mouse livers were characterized A. WT (n=3). B. Pten-/- (n=4). C. Pten-/- Tgfbr2-/- (n=4).

2016-02-26 | E-GEOD-66717 | biostudies-arrayexpress

Transcriptional profiling of mouse prostate tumors with conditional mutations in the Pten, Apc, or Tgfbr2 genes

Project description:We report the changes in gene expression in mouse prostate comparing normal wild type prostate to tumors generated by Cre mediated deletion of Pten or Apc, either with or without deletion of Tgfbr2. Pten single mutant tumors were isolated at either 8 weeks or 22 weeks of age, with high grade prostate intraepithelial neoplasia (HGPIN) as the main phenotype. Pten;Tgfbr2 double mutants were isolated at 8 weeks (primarily HGPIN), or at 11-14 weeks with extensive locally invasive cancer. Apc single mutants were isolated at 36 weeks old with adenosquamous HGPIN, or at 21-24 weeks of age for the Apc:Tgfbr2 double mutants, which had adenosquamous carcinoma. Ages for the two double mutant groups were based on initial signs of excess tumor burden. Wild type control prostates were isolated at around 20 weeks of age.

2018-05-14 | GSE108017 | GEO

RNA sequence data from liver-specific Pten/Traf3 knockout mice

Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a mouse model of cholangiocarcinogenesis by specifically deleting Pten and Traf3 in the liver. RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.

2022-03-31 | GSE178418 | GEO

Single cell RNA sequence data from liver-specific Pten/Traf3 knockout mice

Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a mouse model of cholangiocarcinogenesis by specifically deleting Pten and Traf3 in the liver. single cell RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.

2022-03-31 | GSE178814 | GEO

RNA sequence data from liver-specific Pten/Traf3 knockout mice [HepG2 RNA-seq]

Project description:Intrahepatic cholangiocarcinoma (ICC) is known to have a poor prognosis among primary liver cancers. We created a vitro model of cholangiocarcinogenesis using HepG2 with specifically knockdown of Pten and Traf3. RNA sequence was performed with RNA extracted from the liver of mice lacking liver-specific Pten and Traf3.

2022-03-31 | GSE184276 | GEO

Effect of S534A substitution in the p65 subunit of Nfkb on response to 1mg LPS

Project description:WT mice and Nfkb/p65 S534A were exposed to 1mg/kg LPS and their gene expression measured. Affymetrix Mouse 1.0ST chips were used to measure gene expression.

2017-04-05 | GSE67178 | GEO

Effect of S534A substitution in the p65 subunit of Nfkb on response to 1µg LPS

Project description:WT mice and Nfkb/p65 S534A were exposed to 1µg/kg LPS and their gene expression measured. Affymetrix Mouse 1.0ST chips were used to measure gene expression

2017-04-05 | GSE67072 | GEO

VHL Status Influences Phenotype of Liver Cancers Arising from PTEN Loss

Project description:Background: PTEN loss contributes to the development of many cancers and is associated with both hepatocellular carcinoma and cholangiocarcinoma. The pathogenesis of these malignancies is unclear, but they are speculated to arise from common cellular origins. We explored the influence of secondary effects, like hypoxia signaling, through co-deletion of Pten and Vhl in a murine model.Methods: We used a CreER-linked keratin 18 mouse model to conditionally delete Pten, Vhl or both, evaluating the resultant tumors by histology and gene expression microarray. A cohort of human cholangiocarcinoma samples was evaluated for relationships between HIF-1a expression and clinical outcomes.Results: Both Pten deletion genotypes developed liver tumors, but with differing phenotypes. Pten deletion alone led to large, invasive tumors with widespread hepatosteatosis. Co-deletion of Pten and Vhl resulted in low tumor burden and reduced steatosis. Microarray analysis divided mouse tumors’ respective genotypes by gene expression. This gene expression profile grouped a human tumor cohort according to histologic type with the Pten deletion signature aligning with hepatocellular carcinoma, whereas the Pten; Vhl deletion signature associated with cholangiocarcinomas. In a human cholangiocarcinoma cohort, we observed correlation between HIF-1a expression and overall survival.Conclusions: Pten deletion leads to tumor formation and steatosis in mouse livers. Co-deletion of Vhl and Pten resulted in lower tumor burden with gene expression profiling suggesting a switch from hepatocellular expression features to an expression profile more consistent with cholangiocarinoma. A possible relation between HIF-1a expression and increased overall survival in human cholangiocarcinoma suggests that hypoxia signaling influences tumor phenotype. reference x sample

2014-10-31 | E-GEOD-55874 | biostudies-arrayexpress

VHL Status Influences Phenotype of Liver Cancers Arising from PTEN Loss

2014-10-31 | GSE55874 | GEO

Liver gene expression profiling of transforming growth factor beta receptor 2 heterozygous knockout (Tgfbr2+/-) mice

Project description:Transforming growth factor beta receptor 2 (Tgfbr2) was predicted as a causal gene for abdominal using a novel statistical method named LCMS (Schadt et al., 2005, Nature Genetics). In order to validate this prediction, we profiled the liver tissues of Tgfbr2 heterozygous knockout mice (Tgfbr2+/-) and their littermate wild-type (wt) controls to examine the gene expression signature as well as pathways/networks resulting from the single gene perturbation. 6 Tgfbr2+/- mice and 4 wt controls were profiled. Reference pool included RNA extracted from the liver of 6 wt control mice. Dye-swap was involved in the profiling.

2009-03-07 | E-GEOD-11994 | biostudies-arrayexpress

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