GEO DataSets

Analysis of xenograft tumors generated from independent iKras p53L/+ PDAC cell lines. Cultured parental lines also examined. Doxycycline treatment induced expression of oncogenic KrasG12D. Results provide insight into the molecular mechanisms underlying KrasG12D-mediated PDAC tumor maintenance.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 7 cell line, 3 cell type, 2 protocol sets

Platform:

GPL1261

Series:

GSE32277

33 Samples

Download data: CEL

(Submitter supplied) The maintenance of advanced malignancies relies on continued activity of driver oncogenes, although their rate-limiting role is highly context-dependent with respect to tumor types and associated genetic alterations. Oncogenic Kras mutation is the signature event in human pancreatic ductal adenocarcinoma (PDAC), serving a critical role in tumor initiation. Here, an inducible KrasG12D-driven p53 mutant PDAC mouse model establishes that advanced PDAC remains strictly dependent on continued KrasG12D expression and that KrasG12D serves a vital role in the control of tumor metabolism, through stimulation of glucose uptake and channeling of glucose intermediates through the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway (PPP). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4343

Platform:

GPL1261

33 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

41 Samples

Download data: CEL

(Submitter supplied) Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12D–independent PDAC recurrence. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

5 Samples

Download data: CEL

(Submitter supplied) Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible KrasG12D-driven mouse model of PDAC has established a critical role for sustained KrasG12D expression in tumor maintenance, providing a model to determine the potential for, and underlying mechanisms of, KrasG12D–independent PDAC recurrence. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

36 Samples

Download data: CEL

(Submitter supplied) In this dataset, we include the expression data obtained from KRas expressing tumors, matched Kras expressing tumor spheres, surviving cells and surviving cells after KRas re-expression for 24hs

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

20 Samples

Download data: CEL

(Submitter supplied) USP21 promotes PDAC tumor cells to bypass KRAS* dependency. To dissect the molecular mechanism, we conducted RNA-seq analysis comparing iKPC cancer cells overexpressing GFP, wildtype USP21 and enzyme-dead USP21 at day 3 after KRAS* extinction. KRAS*-expressing iKPC cells with GFP overexpression are positive control.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: TSV

(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

(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

(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

(Submitter supplied) TGFbeta promotes the bypass of KRAS* dependency in PDAC. To dissect the molecular mechanisms that regulated by TGFbeta in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells with or without TGFbeta treatment.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: TSV

(Submitter supplied) KRAS* is required for PDAC tumor mantainence. To dissect the molecular mechanisms that regulated by KRAS* in PDAC tumors, we conducted RNA-seq analysis of KRAS*-expressing iKPC PDAC tumors and iKPC tumors after KRAS* extinction for 24 hours.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

8 Samples

Download data: TSV

(Submitter supplied) HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in escaper cells, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells knocking down of HDAC5 or scramble shRNA control.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

15 Samples

Download data: TSV

(Submitter supplied) HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

9 Samples

Download data: TSV

(Submitter supplied) HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3. To understand the epignetic regulations by HDAC5, we performed ChIP-seq analysis of H3K4me3, H3K27ac and H3K9ac in PDAC cells overexpressing GFP or HDAC5, and in HDAC5 escaper cells with HDAC5 knockdown or scramble control.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

16 Samples

Download data: BW

(Submitter supplied) HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3 to suppess gene expression. To identify the target genes of HDAC5, we performed ChIP-seq analysis in FLAG-tagged HDAC5 PDAC escaper cells. HDAC5 binding chromatins were pulled down by HDAC5 antibody and FLAG antibody as replicates.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

6 Samples

Download data: BED, BW

(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

(Submitter supplied) Almost all human pancreatic ductal adenocarcinomas (PDACs) are driven by oncogenic Kras and the progression of the disease is characterized by the serial appearance of certain genetic lesions. Mouse models have convincingly shown that Kras mutation induces classical PanIN lesions that can progress to PDAC in the appropriate tumor suppressor background. However, the cooperative mechanism between mutant Kras-dependent signaling surrogates and other oncogenic pathways remains to be fully elucidated in order to devise better therapeutic strategy. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4528

Platform:

GPL1261

8 Samples

Download data: CEL

Analysis of primary pancreatic ductal epithelial cells (PDECs) established from 6-week-old Pdx1-Cre;LSL-KrasG12D L/+;Pten L/+ animals. Oncogenic KrasG12D and Pten deficiency cooperate to induce pancreatic ductal adenocarcinoma (PDAC). Results provide insight into molecular basis of PDAC development.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE25828

8 Samples

Download data: CEL

(Submitter supplied) That mutational activation of Kras and inactivation of p16 are two signature genetic alterations required for development of PDAC. To elucidate the downstream pathways activated by oncogenic Kras and inactivated p16 in human pancreatic tumorigenesis, we profiled gene expression in HPNE/Kras/shp16 and HPNE/Kras cells using cDNA microarray analysis.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

1 Sample

Download data: TXT