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Links from GEO DataSets

Items: 20

1.

Orthotopic KI tumors treated with vehicle or IRAK4 inhibitor CA-4948 for two weeks

(Submitter supplied) We treated FVBN/J mice bearing orthotopic KI tumors with vehicle or CA-4948 for two weeks and performed bulk RNASeq to assess transcriptomic changes in the tumor
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE197328
ID:
200197328
2.

scRNAseq of the PDAC tumors from autochtonous KPC mice treated with vehicle or IRAK4 inhibitor CA-4948

(Submitter supplied) We treated 6 week-old KPC mice with vehicle or CA-4948 and perform scRNASeq to assess transcriptomic changes in CAFs and immune cells
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE197329
ID:
200197329
3.

Targeting Focal Adhesion Kinase Renders Pancreatic Cancers Responsive to Checkpoint Immunotherapy

(Submitter supplied) Single-agent immunotherapy has achieved limited clinical benefit to date in patients with pancreatic ductal adenocarcinoma (PDAC). This may be a result of the presence of a uniquely immunosuppressive tumor microenvironment (TME). Critical obstacles to immunotherapy in PDAC tumors include a high number of tumor-associated immunosuppressive cells and a uniquely desmoplastic stroma that functions as a barrier to T cell infiltration. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL21163
12 Samples
Download data: TXT
Series
Accession:
GSE75233
ID:
200075233
4.

Tumor-stroma IL-1β-IRAK4 Feedforward Circuitry Drives Tumor Fibrosis, Chemo-resistance and Poor Prognosis in Pancreatic Cancer

(Submitter supplied) Targeting the desmoplastic stroma of pancreatic ductal adenocarcinoma (PDAC) holds promise to augment the effect of chemotherapy, but so far success remains limited in the clinic. Furthermore, preclinical mouse models suggest that near-depletion of cancer-associated fibroblasts (CAFs) carries a risk of accelerating PDAC progression. These concerns underscore the need to concurrently target the key signaling mechanisms that drive the malignant attributes of both CAFs and PDAC cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10904
24 Samples
Download data: TXT
Series
Accession:
GSE73046
ID:
200073046
5.

Cadherin 11 promotes immunosuppression and extracellular matrix deposition to promote growth of pancreatic tumors and resistance to gemcitabine in mice

(Submitter supplied) Background & Aims: Pancreatic ductal adenocarcinomas (PDAC) are characterized by fibrosis and an abundance of cancer-associated fibroblasts (CAFs). We investigated strategies to disrupt interactions among CAFs, the immune system, and cancer cells, focusing on adhesion molecule cadherin 11 (CDH11), which has been associated with other fibrotic disorders and is expressed by activated fibroblasts. Methods: We compared levels of CDH11 mRNA in human pancreatitis and pancreatic cancer tissues and cells, compared with normal pancreas, and measured levels of CDH11 protein in human and mouse pancreatic lesions and normal tissues. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: TXT
Series
Accession:
GSE157781
ID:
200157781
6.

SCID mT3-2D KPC Tumors and mT3-2D cell lines

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing
Platforms:
GPL22364 GPL21626 GPL21103
26 Samples
Download data: RCC
Series
Accession:
GSE165169
ID:
200165169
7.

WES for WT and SCID mT3-2D KPC Tumors and mT3-2D cell line

(Submitter supplied) To determine the influence of in vivo tumor growth and antitumor immune responses on the generation of tumor neoepitopes, we performed whole exome sequencing (WES) on the mT3-2D cell line, WT tumors and SCID tumors
Organism:
Mus musculus
Type:
Genome variation profiling by high throughput sequencing
Platform:
GPL21103
11 Samples
Download data: XLSX
Series
Accession:
GSE165167
ID:
200165167
8.

RNA-seq for WT and SCID mT3-2D KPC Tumors and mT3-2D cell lines

(Submitter supplied) To investigate how pancreatic malignant epithelial cells responded to anti-tumor T-cell immune responses in vivo, RNA-seq was used to examine the gene expression profiles of the mT3-2D-GFP cell line and FACS sorted mT3-2D-GFP cancer cells isolated from WT and SCID tumors.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
3 Samples
Download data: CSV, XLSX
Series
Accession:
GSE165166
ID:
200165166
9.

Mouse PanCancer Immune Panel on WT and SCID mT3-2D KPC Tumors

(Submitter supplied) To comprehensively assess the immune milieu of WT and SCID mT3-2D tumors, we employed NanoString nCounter immune profiling. The two groups of samples exhibited distinct immune profiles and indicated greater upregulation of immune-related genes in mT3-2D WT tumors than in SCID tumors.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL22364
12 Samples
Download data: RCC, TXT
Series
Accession:
GSE165165
ID:
200165165
10.

Single cell RNA sequencing profiles on whole tumors from a Kras/Rnf43 genetically engineered mouse model of pancreatic adenocarcinoma

(Submitter supplied) We report single cell RNA sequencing of pancreatic enzymatically digested whole, fresh tumors from a genetically engineered mouse model (GEMM) of pancreatic adenocarcinoma. This GEMM consists of pancreas specific expression of oncogenic Kras (Kras-G12D) in addition of homozygous deletion of the ring finger domain (catalytic domain) of Rnf43. This GEMM is termed 'KRC'.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
10 Samples
Download data: TAR
Series
Accession:
GSE188946
ID:
200188946
11.

HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer

(Submitter supplied) We performed HDAC5 knockdown in pancreatic cancer cell line (PANC-1). The expression profiling showed NF-κB signaling as a potential HDAC5 targets and the conclusions were futher validated in vivo and in vitro.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
12.

Exploring the effects of DPP inhibition on the tumor immune landscape using RNAseq

(Submitter supplied) We examined the effects of an oral small molecule DPP inhibitor (BXCL701) on PDAC tumor growth and tumor immune landscape using mT3-2D and Pan02 subcutaneous syngeneic murine models in C57BL/6 mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
42 Samples
Download data: CSV, XLSX
Series
Accession:
GSE173441
ID:
200173441
13.

The tissue factor-thrombin axis drives pancreatic ductal adenocarcinoma through tumor cell-derived PAR-1

(Submitter supplied) RNA-Seq analysis reporting the transcriptional changes induced by treatment of mouse pancreatic ductal adenocarcinoma cell lines with thrombin for 24h
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
24 Samples
Download data: TXT
Series
Accession:
GSE120370
ID:
200120370
14.

Transcriptomic analysis of IRAK4 in murine pancreatic cancer cells (KP2)

(Submitter supplied) We perform CRISPR knockout of IRAK4 usig two different sgRNAs in murine KP2 cells, and then reexpressed murine IRAK4 in these two KO cell lines. We performed RNAseq on wild-type, IRAK4 KO and IRAK4 KO/rescue cell lines to investigate pathways contolled by IRAK4.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE148442
ID:
200148442
15.

mRNA exrpession patterns in response to RelA siRNA

(Submitter supplied) The experiment aims to identify mRNAs regulated in response to RelA overall aim: elucidate the role of CCL20 mediated immune cell recruitment in NF-[gamma]B mediated TRAIL resistance of pancreatic cancer
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
9 Samples
Download data: CEL
Series
Accession:
GSE87287
ID:
200087287
16.

Reshaping the Tumor Microenvironment of KRASG12D Pancreatic Ductal Adenocarcinoma with combined SOS1 and MEK Inhibition for Improved Immunotherapy Response

(Submitter supplied) KRAS inhibitors have demonstrated exciting pre-clinical and clinical responses, although resistance occurs rapidly. Here, we investigate the effects of KRAS-targeting therapies on the tumor microenvironment using a library of KRASG12D, p53 mutant, murine PDAC-derived cell lines (KPCY) to leverage immune-oncology combination strategies for long-term tumor efficacy. Our findings show that SOS1 and MEK inhibitors (SOS1i+MEKi) suppressed tumor growth in syngeneic models and increased intra-tumoral CD8+ T cells without durable responses. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
21 Samples
Download data
Series
Accession:
GSE264527
ID:
200264527
17.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6246 GPL4134
13 Samples
Download data: CEL, TXT
Series
Accession:
GSE33323
ID:
200033323
18.

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

(Submitter supplied) 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.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
12 Samples
Download data: CEL
Series
Accession:
GSE33322
ID:
200033322
19.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL4134
1 Sample
Download data: TXT
Series
Accession:
GSE27478
ID:
200027478
20.

Single-cell RNA sequencing from PiKP-785 cancer cells under 4 treatment conditions: Kras* On, Kras* 3d off, Kras* 5d off, and Kras* On off on

(Submitter supplied) Single-cell RNA sequencing analysis was performed on primary pancreatic ductal adenocarcinoma derrived cell line from PiKP (P48-Cre; R26-rtTa-IRES-EGFP; tetO-LSL-KrasG12D/+; Trp53L/L) murine tumors. In this study we establish that oncogenic Kras is the predominant driver of T cell paucity and myeloid infiltration in the pancreatic tumor microenvironment. Then, we use scRNA seq analysis of cultured PiKP cells with and without Kras* extinction to identify immune related genes involved in driving Kras* mediated immune supression in PDAC.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE201887
ID:
200201887
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