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Links from GEO DataSets

Items: 18

1.

Targeting Stem Cells and Dysplastic Features with Dual MEK/ERK and STAT3 Suppression in Gastric Carcinogenesis

(Submitter supplied) Pre-cancerous metaplasia progression to dysplasiasignificantlyincreases the risk of gastriccancer, and effective targeting strategies forpre-cancerouslesions are currently lacking.Weaimed to identify key signaling pathways critical for stem cell survival and function in dysplasia.Usingmouse and humanmetaplastic and dysplastic organoids, we evaluated responsestoPyrvinium, a putative anti-cancer drug.WhilePyrvinium induced growth arrest in metaplasticorganoids, itinducedcell death in dysplastic organoidsthrough a dual blockade of MEK/ERKand STAT3 signaling pathways. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE240890
ID:
200240890
2.

Single cell analysis of tumors developed from mouse dysplastic stem cells

(Submitter supplied) To investigate whether the CD44v6neg/CD133+/CD166+ dysplastic stem cells are responsible for gastric adenocarcinoma development and cancer cell heterogeneity in the stomach, we used single cell RNA-seq (scRNA-seq) to examine gene expression profiles of heterogenous cancer cells in two types of gastric adenocarcinoma, cystic type and tubular type, developed from the dysplastic stem cell injection under the skin of immunodeficient nude mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
2 Samples
Download data: TXT
Series
Accession:
GSE202192
ID:
200202192
3.

Comparison of transcriptomic profiles between dysplastic stem cell subpopulations

(Submitter supplied) To investigate transcriptomic profiles of of two dysplastic stem cell (DSC) subpopulations, CD44v6neg/CD133+/CD166+ (DP-DSC) and CD44v6+/CD133+/CD166+ (TP-DSC), in dysplastic organoids (Meta4 organoids) established from active-Kras induced mouse stomachs
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: TXT
Series
Accession:
GSE202191
ID:
200202191
4.

Gastric organoid single-cell RNA-seq

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: CSV
Series
Accession:
GSE121940
ID:
200121940
5.

Gastric organoid single-cell RNA-seq II

(Submitter supplied) Meta4 gastric organoids from Mist1-creERT2/+;KrasLSL/+ mice treated with vehicle or Selumetinib
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
2 Samples
Download data: CSV
Series
Accession:
GSE121939
ID:
200121939
6.

Gastric organoid single-cell RNA-seq I

(Submitter supplied) Meta3 and Meta4 gastric organoids from Mist1-creERT2/+;KrasLSL/+ mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
2 Samples
Download data: CSV
Series
Accession:
GSE121937
ID:
200121937
7.

Induction of gastric cancer by successive oncogenic activation in the corpus

(Submitter supplied) Background & Aims: Metaplasia and dysplasia in the corpus are reportedly derived from dedifferentiation of chief cells. However, the cellular origin of metaplasia and cancer remained uncertain. Therefore, we investigated whether pepsinogen Ctranscript expressing cells (PGC-transcript expressing cells) represent the cellular origin of metaplasia and cancer using a novel Pgc-specific CreERT2 recombinase mouse model. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
6 Samples
Download data: TXT
Series
Accession:
GSE166904
ID:
200166904
8.

Spatial transcriptome analysis of gastric cancer which GAN-KP transplanted C57BL/6J mouse

(Submitter supplied) We have now developed an organoid-based model of gastric cancer from GAstric Neoplasia (GAN) mice, which express Wnt1 and the enzymes COX2 and microsomal prostaglandin E synthase 1 in the stomach. Both p53 knockout (GAN-p53KO) organoids and KRASG12V-expressing GAN-p53KO (GAN-KP) organoids were generated by genetic manipulation of GAN mouse–derived tumor (GAN-WT) organoids. To uncover the molecular mechanism underlying the intratumoral heterogeneity of GAN-KP tumors, we performed spatial transcriptomics analysis with the 10× Genomics Visium platform, which allows characterization of the spatial topography of gene expression.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
1 Sample
Download data: CSV, H5, JSON, PNG
Series
Accession:
GSE186290
ID:
200186290
9.

Gene expression analysis of three tumor organoids (GAN-WT, GAN-p53 and GAN-KP) derived from gastric tumor in K19-Wnt1/C2mE (GAN) mouse.

(Submitter supplied) To develop a syngeneic mouse model of metastatic gastric cancer, we established the tumor organoids from gastric tumor arising in GAstric Neoplasia (GAN) mice (GAN-WT) which express Wnt1 and the PGE2 synthesis enzymes COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) in the stomach epithelium. Furthemore, GAN-WT organoids were genetically manupilated into p53 knockout organoids (GAN-p53KO) and KrasG12V-expressing GAN-p53KO organoids (GAN-KP).
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21163
12 Samples
Download data: TXT
Series
Accession:
GSE178087
ID:
200178087
10.

A Point Mutation R122C in RUNX3 Promotes the Expansion of Isthmus Stem Cells and Inhibits Their Differentiation in the Stomach

(Submitter supplied) Background & Aims: RUNX transcription factors play pivotal roles in embryonic development and neoplasia. We previously identified the single missense mutation R122C in RUNX3 from human gastric cancer. However, how RUNX3R122C mutation disrupts stem cell homeostasis and promotes gastric carcinogenesis remained unclear. Methods: To understand the oncogenic nature of this mutation in vivo, we generated the RUNX3R122C knock-in mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
10 Samples
Download data: XLSX
Series
Accession:
GSE190506
ID:
200190506
11.

A Point Mutation R122C in RUNX3 Promotes the Expansion of Isthmus Stem Cells and Inhibits Their Differentiation in the Stomach

(Submitter supplied) Background & Aims: RUNX transcription factors play pivotal roles in embryonic development and neoplasia. We previously identified the single missense mutation R122C in RUNX3 from human gastric cancer. However, how RUNX3R122C mutation disrupts stem cell homeostasis and promotes gastric carcinogenesis remained unclear. Methods: To understand the oncogenic nature of this mutation in vivo, we generated the RUNX3R122C knock-in mice. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28457
6 Samples
Download data: XLSX
Series
Accession:
GSE190081
ID:
200190081
12.

Gene expression in gastric Mist1+ cells.

(Submitter supplied) Mist1+ cells and parietal cells in mouse stomach were separatedly sorted, and RNAs were isolated. Mist1 (also known as Bhlha15) is expressed in gastric chief cells and gastric stem cells in mice. However, more specific genes for each population needs to be identified to better understand the precise biology in these cell populations. In order to address cell specific gene signature, we separately sorted Mist1+ gastric chief cells and Mist1+ gastric stem cells by FACS, and performed microarray analysis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL
Series
Accession:
GSE133205
ID:
200133205
13.

Inhibition of Met results in concomitant inhibition of Akt and STAT3 signaling pathways, while abrogation of negative feedback permits Erk reactivation

(Submitter supplied) Amplification and activation of the Met receptor tyrosine kinase occurs up to 23% of gastric cancers, suggesting that Met is a therapeutic target in these cancers. However, the steady-state signaling events that occur during chronic Met activation, and mechanisms for resistance to Met small-molecule inhibitors, are poorly understood. Here we show that multiple gastric cancer cell lines harboring MET amplifications are dependent on Met signaling for proliferation and anchorage-independent growth. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
132 Samples
Download data: TXT
Series
Accession:
GSE54532
ID:
200054532
14.

Single cell RNA sequence of liver tumors in hepatocyte-specific Kras mutant mice.

(Submitter supplied) Tumor consisting cells in hepatocyte-specific Kras mutant mice were classified as tumor cells and stromal cells including macrophages, hepatic stellate cells, endothelial cells, and so on. Positive cells for STAT3-target genes, Il-6 family cytokines, and connective tissue growth factor were elucidated.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28457
2 Samples
Download data: CSV
Series
Accession:
GSE192697
ID:
200192697
15.

A subset of metastatic pancreatic ductal adenocarcinomas depends quantitatively on oncogenic Kras/Mek/Erk-induced hyperactive mTOR signalling

(Submitter supplied) Objective Oncogenic Kras-activated robust Mek/Erk signals phosphorylate to the tuberous sclerosis complex (Tsc) and deactivates mammalian target of rapamycin (mTOR) suppression in pancreatic ductal adenocarcinoma (PDAC); however, Mek and mTOR inhibitors alone have demonstrated minimal clinical antitumor activity. Design We generated transgenic mouse models in which mTOR was hyperactivated either through the Kras/Mek/Erk cascade, by loss of Pten or through Tsc1 haploinsufficiency. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
22 Samples
Download data: CEL
Series
Accession:
GSE48643
ID:
200048643
16.

Hyperplastic gastric tumor of K19-C2mE transgenic mouse

(Submitter supplied) Cyclooxygenase-2 (COX-2), the rate-limiting enzyme for prostanoid biosynthesis, plays a key role in gastrointestinal carcinogenesis. Among various prostanoids, prostaglandin E2 (PGE2) appears to be most responsible for cancer development. To investigate the role of PGE2 in gastric tumorigenesis, we constructed transgenic mice simultaneously expressing COX-2 and microsomal prostaglandin E synthase (mPGES)-1 in the gastric epithelial cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL3264
3 Samples
Download data
Series
Accession:
GSE3903
ID:
200003903
17.

Cell type-dependent differential activation of ERK by oncogenic KRAS in human colon cancer and mouse intestinal epithelium

(Submitter supplied) Mutations activating the KRAS GTPase or the BRAF kinase are frequent in colorectal cancer and are thought to constitutively activate the terminal mitogen-activated protein kinase, ERK. Using mass cytometry, we found graded phosphorylation of ERK anti-correlated with cell differentiation in patient-derived colorectal cancer organoids, and unexpectedly this gradient was observed independently of KRAS mutational status. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: TSV
Series
Accession:
GSE115242
ID:
200115242
18.

Oncogenic KRAS(G12V) and BRAF(V600E) in intestinal organoids

(Submitter supplied) Goals of the study was to compare transcripional and phenotypic response of mouse intestinal organoid cultures to the KRAS(G12V) or BRAF(V600E)oncogenes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE115234
ID:
200115234
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