Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of mouse mucinous lung tumors

ABSTRACT: Transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice. We used microarrays to detail the global program of gene expression underlying development of mucinous lung tumors and identified distinct classes of up-regulated genes during this process.

ORGANISM(S): Mus musculus

PROVIDER: GSE40508 | GEO | 2012/08/31

SECONDARY ACCESSION(S): PRJNA174191

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data of mouse mucinous lung tumors

Project description:Transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice. We used microarrays to detail the global program of gene expression underlying development of mucinous lung tumors and identified distinct classes of up-regulated genes during this process. mRNAs were isolated from the whole lungs of the transgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) after 2 months doxycycline administration and hybridized on Affymetrix microarrays. We sought to identify genes induced in mucinous lung tumors.

2012-08-31 | E-GEOD-40508 | biostudies-arrayexpress

The Effect of GATA6 on miRNA in Lung Development

Project description:Gata6 regulates lung epithelial stem cell development and airway regeneration. Here, the expression profile of microRNA was investigated when Gata6 was depleted during lung development. Analysis used total RNA from Sftpc-rtTA:tetO-cre lungs at E14.5 as control samples (WT) for comparison to the experimental samples of total RNA from Gata6flox/flox: Sftpc-rtTA: tetO-Cre mutant lungs at E14.5.

2011-03-01 | E-GEOD-25874 | biostudies-arrayexpress

RNA-seq analysis of Mst1/2 deleted bronchiolar epithelial cells from adult mouse lungs

Project description:Mst1 and Mst2 were conditionally deleted from non-ciliated bronchiolar epithelial cells in the mature lung. Bronchiolar epithelial cells from control and Mst1/2 deleted mice were isolated by cell sorting and used for RNA-seq analysis. Scgb1a1-rtTA/tetO-Cre/Mst1;2-flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from non-ciliated, secretory bronchiolar epithelial cells. Adult mice were maintained on doxycycline food for 16 days to induce deletion of Mst1/2. Lin-/CD326+/CD24-intermediate cells were isolated by fluorescence cell sorting to enrich for the targeted airway epithelial cells. mRNA isolated from Lin-/CD326+/CD24-intermediate cells from control and Mst1/2 D/D mice was pooled and analyzed by RNA-seq to identify transcriptional changes following deletion of Mst1 and Mst2 from mature lung bronchiolar epithelial cells.

2015-01-01 | E-GEOD-61627 | biostudies-arrayexpress

Effect of mutant GNAS expression in the doxycycline-inducible Kras;Gnas mouse model of IPMN using scRNA-seq

Project description:We investigated the effect of GNAS(R201C) expression in the Kras;Gnas model of pancreatic intraductal papillary mucinous neoplasms where transgenic mutant GNAS is doxycycline inducible (LGKC; p48(Cre), Kras(LSL-G12D), Rosa26(LSL-rtTA)), Tg(TetO-GNAS(R201C)) using scRNA-seq of dissociated pancreatic tissues.

2024-09-15 | GSE275404 | GEO

FiTAc-seq analysis of PDX 14-07 and MMTV-rtTA/tetO/Her2 tumors treated with abemaciclib

Project description:We measured changes in H3K27ac after treatment of PDX 14-07 or MMTV-rtTA/tetO-Her2 tumors implanted in nude mice with abemaciclib

2020-09-03 | GSE157384 | GEO

Effect of mutant GNAS expression in doxycycline-inducible murine pancreatic cancer cell lines

Project description:We investigated the transcriptomic effect of GNAS(R201C) expression in murine cell lines derived from the Kras;Gnas model of pancreatic intraductal papillary mucinous neoplasms where transgenic mutant GNAS is doxycycline inducible (LGKC; p48(Cre), Kras(LSL-G12D), Rosa26(LSL-rtTA)), Tg(TetO-GNAS(R201C)) using bulk RNA-seq.

2024-09-15 | GSE275403 | GEO

Nkx2.1 represses a latent gastric differentiation program in lung adenocarcinoma

Project description:During cancer evolution, cellular differentiation programs become dysregulated. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 results in transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs may be required for tumors to reach a primitive, dedifferentiated state. The study was designed to compare the expression profiles of Nkx2-1-positive lung adenocarcinomas with tumors in which Nkx2-1 was deleted at the time of initiation or 6-7 months after initiation.

2013-04-10 | E-GEOD-36473 | biostudies-arrayexpress

Nkx2-1 Represses a Latent Gastric Differentiation Program in Lung Adenocarcinoma

Project description:Tissue-specific differentiation programs become dysregulated during cancer evolution. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and by inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 causes transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs are required for tumors to reach a primitive, dedifferentiated state. ChIP-seq data from murine lung adenocarcinomas on (i) transcription factors Nkx2-1 and Foxa in Nkx2-1-deleted tumors and Nkx2-1-positive control tumors, and (ii) four histone marks in Nkx2-1-deleted tumors and Nkx2-1-positive control tumors. (All samples in duplicate and with input controls, i.e. (2 x [(3+3) + (2+8)]) - 1 = 31 samples total - 1 input control used for transcription factor and histone mark, GSM1059357)

2013-04-09 | E-GEOD-43252 | biostudies-arrayexpress

Therapeutic efficacy of INX-315, a selective CDK2 inhibitor, in solid tumors [HER2mouse upfront RNAseq]

Project description:We treated tumour-bearing MMTV-rtTA/tetO-HER2 female mice with either vehicle (veh), INX-315 (INX), Abemaciclib (LY) or both INX-315 and Abema in combination (LY.INX) for 7 days. Resistant tumors were collected and RNA sequencing performed

2023-11-22 | GSE243149 | GEO

Nkx2-1 Represses a Latent Gastric Differentiation Program in Lung Adenocarcinoma

2013-04-09 | GSE43252 | GEO