Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles of spontaneous metastasis in a K-ras/p53 mutant mouse model

ABSTRACT: The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. We identified 2,209 genes that were differentially expressed in distant metastases relative to matched lung tumors. Mining of publicly available data bases revealed this expression signature in a subset of NSCLC patients who had a poorer prognosis than those without the signature.

ORGANISM(S): Mus musculus

PROVIDER: GSE14449 | GEO | 2009/04/15

SECONDARY ACCESSION(S): PRJNA114501

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiles of spontaneous metastasis in a K-ras/p53 mutant mouse model

2009-04-14 | E-GEOD-14449 | biostudies-arrayexpress

Gene expression profiles of 344SQ lung adenocarcinoma cells with high metastatic potential (syngeneic mouse model)

2009-11-10 | GSE14458 | GEO

Transcription profiling of mouse 344SQ lung adenocarcinoma cells with high metastatic potential (syngeneic mouse model)

Project description:The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. As a tool to investigate the biologic basis for metastasis in this model and to query the roles of specific genes in this signature, we isolated adenocarcinoma cell lines from these mice and used them to develop a syngeneic tumor model in wild-type littermates. Transcriptional profiling of the highly metastatic subcutaneous tumors revealed genes that regulate, among other processes, epithelial-to-mesenchymal transition and intra-tumoral inflammation and angiogenesis, whereas the non-metastatic tumors did not. Experiment Overall Design: Cell lines from p53R172Hâg/+ K-rasLA1/+ mice were derived from tumor tissues removed at autopsy from two different mice (#344 and #393). The tissues were minced, placed in culture, and passed serially in RPMI 1640 supplemented with 10% fetal bovine serum (FBS), which yielded mass populations of tumor cells derived from primary lung tumors (344P and 393P), mediastinal lymph nodes (344LN and 393LN), and a subcutaneous site (344SQ). Syngeneic tumors were isolated, carefully dissected to remove the adjacent tissue, snap-frozen in liquid nitrogen and stored at -80Â° until use. Part of each dissected tumor was histologically evaluated by a board-certified pathologist. Snap-frozen samples were processed and analyzed on Affymetrix Mouse Expression Array 430A 2.0 chips. Experiment Overall Design: Expression profiling performed on 344SQ, 393P, and 393LN

2009-11-28 | E-GEOD-14458 | biostudies-arrayexpress

Mouse oral tumors induced by activation of Ras and p53 mutations

Project description:The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared the expression profiles of oral tumors induced by activation of oncogenic K-ras and p53 gain- or loss-of-function mutations Oral tumors were induced by activation of endogenous oncogenic K-rasG12D and p53 loss- or gain-of-function mutations (p53R172H) Oral tumors from mice carrying the p53R172H mutation or deletion of p53 were collected for gene expression analysis

2012-03-30 | E-GEOD-28203 | biostudies-arrayexpress

Mouse oral tumors induced by activation of Ras and p53 mutations

2012-03-31 | GSE28203 | GEO

Characterization of the genetic mouse model of non-small cells lung cancer p53R172H∆g/KrasG12D

Project description:Background: Non-small cell lung cancer (NSCLC) accounts for 81% of all cases of lung cancer and they are often fatal because 60% of the patients are diagnosed at an advanced stage. Besides the need for earlier diagnosis, there is a great need for additional effective therapies. In this work we investigated the feasibility of a lung cancer progression mouse model, mimicking features of human aggressive NSCLC cancer, as biological reservoir for potential therapeutic targets and biomarkers. Results:RNA-seq profiling was performed on total RNA extracted from lungs of 30 week-old p53R172H∆g/KrasG12D and wild type mice to detect fusion genes and gene/exon-level differential expression associated to the increase of tumor mass. Fusion events were not detected in p53R172H∆g/KrasG12D tumors. Differential expression at exon-level detected 33 genes with differential exon usage. The study provides a complete transcription overview of the p53R172H∆g/KrasG12D mouse NSCLC model

2013-09-25 | GSE51144 | GEO

Global gene expression profiling of shLUC (control) and shMLL4-1 and shMLL4-3 (MLL4-knockdown) LKR-10 mouse lung cancer cell using RNA sequencing

Project description:Here, we show that the histone H3 lysine (H3K4) methyltransferase MLL4 (a COMPASS/SET1-like enzyme; also called KMT2D) is ranked the most highly inactivated epigenetic modifier in NSCLC tumors lung-specific loss of Mll4 accelerates K-RasG12D-induced lung tumorigenesis in mice while reducing their survival time. Mll4 loss upregulated tumor-promoting programs, such as glycolysis, which is also enriched in human lung tumors with low MLL4 levels or MLL4 inactivation. The inhibition of glycolysis selectively impeded the proliferation and tumorigenic growth of NSCLC cells bearing human MLL4-inactivating mutation. Mll4 loss caused widespread impairment of super-enhancer signals, including super-enhancer associated with the circadian transcriptional repressor gene Per2 which represses glycolysis genes in NSCLC cells.

2020-04-13 | GSE143498 | GEO

Genome-wide maps of chromatin state in K-RasLSL-G12D and K-RasLSL-G12D;Mll4fl/fl induced lung tumors in mice

2020-04-13 | GSE116659 | GEO

Global gene expression profiling of K-RasLSL-G12D and K-RasLSL-G12D;Mll4fl/fl lung tumors using RNA sequencing

2020-04-13 | GSE116658 | GEO

Differentially-expressed-transcriptome study of Non-Small Cell Lung Carcinoma

Project description:We systematically profiled the genome-wide alternative splicing events in Lung Adenocarcinoma (LUAD) and Lung Squomous Cell Carcinoma (LUSC) against Lung Control through Human Transcriptome Array2.0. Non-invasive Stage IIIA non-small cell lung cancer (NSCLC) is heterogeneous in nature which makes it difficult to predict, diagnose and prognose owing to lower 5-year survival rate and 75-85% brain or bone metastasis. Hence, we hypothesized to develop transcript-based signature to categorize Stage IIIA-NSCLC-LUAD and LUSC, as well as identify markers which could indicate towards prognosis of disease. We were able to molecularly-categorize LUAD- and LUSC-tissue more precisely through HTA array2.0.

2020-09-21 | GSE138682 | 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