Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene Expression Differences in MYC and RAS Driven Liver Cancer Transgenic

ABSTRACT: MYC and RAS signaling are two oncogene pathways important in human liver cancer. We sought to model liver cancer driven by either MYC or RAS using conditional LAP-tTA crossed to either TRE-MYC or TRE-HRAS models in the FVB/N background, and to understand oncogenic signaling pathways that are distinct between each model. Non-tumor tissue, from LAP-tTTA (LT2) mice were used as controls. In this study, we generated tumors from either MYC or RAS driven tumors and compared global gene expression changes to each other and control samples.

ORGANISM(S): Mus musculus

PROVIDER: GSE73295 | GEO | 2018/09/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene Expression Analysis of Transgenic Myc-Driven Liver Tumor Formation and Regression

Project description:Gene expression changes were examined in transgenic MYC-driven liver cancers at different time points as tumors formed and upon early regression. Time points evaluated include: Control (non-tumor bearing), Pre-tumor (mice were removed from doxyclycine in their diet to induce MYC oncogene expression for 4-5 weeks), Tumor (tumor nodules from mice that had been off of doxycycline for 8-9 weeks) and Early tumor regression (tumor-bearing mice were placed back on doxycycline for 72 hrs to inhibit MYC oncogene expresion). MYC-Driven Mouse Tumor Models are described in Schahaf, et al., Nature, 2004 and Goga, et al., Nature Medicine, 2007. 11 Total Samples: 3 Control, 4 Pre-Tumor, 4 Tumor, 4 Early Tumor Regression. Control = LAP-tTA transgenic mice. Others = TRE-MYC x LAP-tTA double transgenic mice (doxy off).

2011-07-06 | E-GEOD-28198 | biostudies-arrayexpress

MYC-driven mouse HCC proteomics

Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").

2022-10-12 | PXD031478 | Pride

Gene expression profile of c-MYC driven mouse liver tumours, compared with Normal livers from control mice

Project description:Liver tumours are induced by overexpresion of human c-MYC (LAP-tTA/tet-o-MYC) Using Affymetrix microarrays we compared gene expression of both tissues

2020-03-27 | GSE129013 | GEO

Study of gene expression of mouse cMET experiments

Project description:We analyzed the molecular changes in a mouse c-MET over-expression model of hepatocellular carcinoma (HCC). FVB mice overexpressing human c-MET carried one copy of the LAP-tTa transgene (the liver-specific LAP promoter driving the Tet-VP16 transactivator) and one copy of the TRE-c-MET transgene (Tet-operator regulated human c-MET gene). Normal liver or liver tumor tissue (two per mouse) was collected and processed for gene expression profiling.

2011-08-14 | E-GEOD-25142 | biostudies-arrayexpress

RNA-seq of heart tissue from 15 day old mice 4 hours post MycER activation compared to wild type controls. RNA-seq of heart tissues from adult mice that have expressed oncogenic H-Ras for 4 weeks followed by MycER activation for 4 hours compared to MycER negative controls.

Project description:Aim: To determine RNA expression levels in the heart of mice 4 hours post Myc activation. Hearts were isolated from 15 day old wild-type (R26+/+) and R26CAG-c-MycERT2/+ mice following 4 hours of MycER activation via administration of (Z)-4-hydroxytamoxifen. Hearts were isolated from adult TetO-HRas; Myh6-tTA; R26CAG-c-MycERT2/+ and TetO-HRas; Myh6-tTA following 4 weeks of oncogenic H-Ras activation (Doxycycline withdrawal) and following 4 hours of MycER activation via administration of (Z)-4-hydroxytamoxifen.

2020-02-24 | E-MTAB-7595 | biostudies-arrayexpress

miRNA expression changes in murine liver tumorigenesis

Project description:Hepatocellular carcinoma (HCC) is associated with poor survival for patients and few effective treatment options, raising the need for novel therapeutic strategies. MicroRNAs (miRNAs) play important roles in tumor development and show deregulated patterns of expression in HCC. Because of the liver’s unique affinity for small nucleic acids, miRNA based therapy has been proposed in the treatment of liver disease. There is thus an urgent need to identify and characterize aberrantly expressed miRNAs in HCC. In our study, we profiled miRNA expression changes in de novo liver tumors driven by MYC and/or RAS, two canonical oncogenes activated in a majority of human HCC. RNA from normal liver (LT2) and tumor tissue (LT2/MYC, LT2/RAS, LT2/MYC/RAS) was extracted, enriched for miRNAs and biotin-labeled using Ambion’s miRVana, flashPAGE and miRVana miRNA labeling kits respectively. Samples (n=4) from each genotype were hybridized to a custom Affymetrix Genechip designed to miRNA probes derived from Sanger miRBase v9.2. This array contained a total of 14216 probes, of which 672 matched to 301 unique mouse miRNAs. For each probe, an estimated background value was subtracted that was derived from the median signal of a set of GC-matched anti-genomic controls. Detection calls were based on a Wilcoxon rank-sum test of the miRNA probe signal compared to the distribution of signals from GC-content matched anti-genomic probes and normalized according to the variance stabilization method described.Post-normalized data scale is reported as generalized log2 data. For statistical hypothesis testing, one-way ANOVA was applied and probes are considered significantly differentially expressed based on a default p-value of 0.05 and log2 difference >1 or <-1.

2013-09-01 | E-GEOD-44570 | biostudies-arrayexpress

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

Project description:Identification of critical survival determinants of PDGF-driven proneural glioma. Results provided information about the genes and pathways that are regulated by PDGF signaling in PDGF-driven proneural glioma and led to the assessment of the importance of the USP1-ID2 axis in proneural glioma. Total RNA obtained from PDGF-driven glioma spheroid cells (PDGF-GSC) and primary tumors arising in the Gfap-tTa/Tre-PDGFB mouse model used in our study was analyzed to determine to which subtype of GBM these specimens belonged.

2016-03-22 | E-GEOD-77423 | biostudies-arrayexpress

scRNAseq of TAZ-CAMTA1 expressing endothelial cells in vivo

Project description:TAZ-CAMTA1 is a defining genetic aberration in the vascular cancer epithelioid hemangioendothelioma. We generated a novel transgenic mouse that expresses TAZ-CAMTA1 in endothelial cells. These mice develop vascular tumors in the lung and die by average on day 40. We isolated GFP + endothelial cells from three five-week old TRE-TAZ-CAMTA1;Cdh5-tTA;TRE-GFP mice and subjected these endothelial cells to scRNA-seq via the 10X genomics platform

2021-05-23 | GSE156803 | GEO

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells following Ikaros restoration

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells isolated from two untreated and two 3-day Dox-treated mice.

2015-02-02 | E-GEOD-64899 | biostudies-arrayexpress

Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis

Project description:Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in recent years in developed nations1,2. The MYC oncogene or its paralogs are frequently amplified or overexpressed in particularly aggressive subtypes of cancer associated with stem cell-like features and worse clinical outcomes3,4, including in liver cancer5. Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent and S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues methionine depletion. A low methionine diet, or the methylation inhibitor 5-azacytidine limited MYC-driven tumor formation, but RAS-driven liver cancer was resistant to a low methionine diet. Metabolic tracing of methionine catabolism in MYC high cells identified increased m5C methylation of genomic DNA or ribosomal RNA. We identified NOP2, an rRNA m5C-methyltransferase as a MYC target gene. Knockdown of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumorigenesis. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and NOP2 may serve as a new therapeutic target in liver cancer.

2022-10-06 | GSE214724 | 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