Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq single cells analysis of 2 tumors from KPC (KrasLSL-G12D/+ Trp53LSL-R172H/+ Pdx1-Cre) mice

ABSTRACT: RNA-seq single cells analysis of 2 tumors from KPC (KrasLSL-G12D/+ Trp53LSL-R172H/+ Pdx1-Cre) mice

PROVIDER: PRJNA471312 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

2012-01-24 | E-GEOD-33322 | biostudies-arrayexpress

Gene expression differences between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice

Project description:Constitutive Kras and NF-kappaB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). However, the mechanisms of constitutive NF-kappaB activation in KrasG12D-induced PDAC are not yet understood. Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kappaB activation and completely suppressed PDAC development in KrasG12D and KrasG12D;Ink4a/Arf mutant mice, demonstrating a genetic link between IKK2/beta and KrasG12D in PDAC inception. Our findings reveal that KrasG12D-activated AP-1 induces IL-1alpha, which in turn activates NF-kappaB and its target genes IL-1alpha and p62, to initiate IL-1alpha/p62 feedforward loops for inducing and sustaining NF-kappaB activity. Furthermore, IL-1alpha overexpression correlates with Kras mutation, constitutive NF-kappaB activity, and poor survival in PDAC patients. Therefore, our findings establish a pathway linking duel feedforward loops of IL-1alpha/p62 through which IKK2/beta/NF-kappaB is activated by KrasG12D. To study Kras-induced inflammatory responses and to identify differentially expressed genes between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice, cDNA microarray analysis was performed.

2012-01-24 | E-GEOD-27478 | biostudies-arrayexpress

mRNA transcriptome sequencing of CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Tp53fl/fl and KrasLSL-G12D/+Tp53fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre

Project description:Comparative gene expression profiling analysis of RNA-seq data in CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Tp53fl/fl and KrasLSL-G12D/+Tp53fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre.

2024-01-01 | GSE250082 | GEO

mRNA transcriptome sequencing of CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Lkb1fl/fl and KrasLSL-G12D/+Lkb1fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre

Project description:Comparative gene expression profiling analysis of RNA-seq data in CD45- lung tumor cells from tumor-burdened lungs of KrasLSL-G12D/+Lkb1fl/fl and KrasLSL-G12D/+Lkb1fl/flUsp25-/- mice 10 weeks after they were intranasally injected with Ad-Cre.

2024-01-01 | GSE250081 | GEO

Murine models of pancreatic cancer: KPC

Project description:We harvested and sequenced the spontaneous pancreatic tumor generated by a 6-month-old KPC mouse (KrasLSL-G12D; Trp53LSL-R172H; Ptf1a-Cre).

2022-10-04 | GSE202651 | GEO

Kras-induced ikk2/nf-kappaB activation by IL-1 alpha and p62 freedforward loops is required for development of pancreatic ductal adenocarcinoma

Project description:This SuperSeries is composed of the following subset Series: GSE27478: Gene expression differences between the pancreatic tissues of Pdx1-Cre;KrasLSL-G12D and Pdx1-Cre;KrasLSL-G12D;IKK2/betaF/F mice GSE33322: Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice Refer to individual Series

2012-01-24 | E-GEOD-33323 | biostudies-arrayexpress

RNA-SEQ analysis of pancreatic ductal adenocarcinoma tumours in Pdx1-Cre;lsl-KRas[G12D] (KC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC), Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];c-Myc[fl/+] (KMC-Mycfl/+), and Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM];Zbtb17[fl/fl] mice (KMC-Miz1fl/fl)

Project description:Activation of endogenously expressed KRas[G12D] in the pancreas of mice gives rise primarily to early stage PanIN lesions, however such lesions can occasionally progress to end-stage ductal adenocarcinoma (PDAC). Progression of KRas[G12D]- initiated lesions to PDAC is accelerated by modest expression of MYC from the Rosa26 locus. Deletion of 1 copy of endogenous c-Myc or both copies of endogenous Zbtb17 (aka Miz1), slows progression to PDAC and extends healthful survival of Pdx1-Cre;lsl-KRas[G12D];Rosa26-lsl-MYC[DM] (KMC) mice. Tumours were removed from mice with all 4 genotypes and validated by histological examination prior to RNA-SEQ analysis.

2020-03-16 | E-MTAB-8797 | biostudies-arrayexpress

Enhancer activation during tumor progression in the KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma.

Project description:Murine pancreatic ductal adenocarcinoma tumor organoids (T6 and T23) were generated from primary tumors from KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre mice. At the first passage, cells in Matrigel were overlaid with mouse complete medium alone or supplemented with 10 uM Nutlin-3a to select for cells that have undergone loss-of-heterozygosity (LOH) for the wild-type (wt, "+") allele of Trp53. Organoids were cultured for 3 passages in the presence or absense of Nutlin-3a, and then culturing was continued in unsupplemented mouse complete medium. H3K27ac ChIP-sequencing (ChIP-seq) was performed to identify regions differentially enriched for H3K27ac binding in Trp53-LOH vs. wt tumor organoids.

2020-06-16 | GSE144704 | GEO

RNA-seq single cells analysis of 2 tumors from KPC (KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre) mice

Project description:We investigated the RNA expression levels of NF-kB ligands and their receptors in epithelial cancer cells and cancer-associated fibroblasts (CAFs) from KPC tumors

2018-12-26 | GSE114417 | GEO

Single-cell analysis of murine pancreatic ductal adenocarcinoma cells reveals the transcriptional dynamics of pancreatic cancer progression..

Project description:This study used 10X Genomics, single-cell RNA-sequencing to examine the differentiation states of cancer cells present in tumors derived from the KrasLSL-G12D; Trp53LSL-R172H; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma. The study analyzed tumors from 8 different mice.

2024-01-29 | GSE195914 | 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