Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

ABSTRACT: Our studies indicate that cancer cells of carcinomas are coated with CXCL12 chemokine in covalent conjugation with keratin-19 (KRT19). Murine pancreatic ductal adenocarcinomas (PDA) formed with Krt19-edited cancer cells lack the CXCL12-coating and are infiltrated with T cells, compared to tumors formed with control sgScramble PDA cells. To probe the immunological role of this CXCL12-coating thoroughly, bulk RNA sequencing of subcutaneous (s/c) murine sgScramble PDA tumors and Krt19-edited PDA tumors were conducted. As comparison, an immunogenic tumor model was also assessed. To do so, s/c sgScramble PDA tumors and PDA tumors formed with sgScramble cells exppressing doxcycline-inducible ovalbumin (icOVA) were harvested and processed for bulk RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE192853 | GEO | 2022/01/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

Project description:Our studies indicate that cancer cells of carcinomas are coated with CXCL12 chemokine in covalent conjugation with keratin-19 (KRT19). Murine pancreatic ductal adenocarcinomas (PDA) formed with Krt19-edited cancer cells lack the CXCL12-coating and are infiltrated with T cells, compared to tumors formed with control sgScramble PDA cells. To probe the immunological role of this CXCL12-coating thoroughly, bulk RNA sequencing of subcutaneous (s/c) murine sgScramble PDA tumors and Krt19-edited PDA tumors were conducted.

2022-01-07 | GSE193027 | GEO

The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

Project description:The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

| PRJNA794150 | ENA

The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

Project description:The immunological comparison of control PDA tumors and Krt19-edited PDA tumors

| PRJNA793450 | ENA

Pervasive subtypes of pancreatic ductal adenocarcinoma (PDA) and their differing response to therapy.

Project description:Pancreatic ductal adenocarcinoma (PDA) carries a dismal prognosis and current treatments are only modestly effective. We present evidence that this variation is caused in part by recurrent, pervasive molecular differences between tumors. mRNA expression profiles measured using microdissected PDA clinical samples reveal three dominant subtypes of disease; epithelial, mesenchymal and acinar-like. The classical and quasi-mesenchymal subtypes are observed in human and mouse PDA cell lines. Importantly, responses to cytotoxics and KRAS depletion in human PDA cell lines differ substantially between subtypes, and in opposing directions. Integrated genomics implicate and functional studies support overexpression of the trancription factor GATA6 as a driver of the epithelial subtype. These results provide a molecular framework for evaluating the prospects of personalized treatment in PDA. RNA was extracted from archival patient FFPE PDA samples and hybridized on Affymetrix U133 plus 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA. RNA was extracted from human PDA cell line samples and hybridized on Affymetrix U133 plus 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA. RNA was extracted from mouse PDA cell lines and hybridized on Affymetrix Mouse 430a 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA.

2011-04-01 | E-GEOD-17891 | biostudies-arrayexpress

Pervasive subtypes of pancreatic ductal adenocarcinoma (PDA) and their differing response to therapy.

2011-04-01 | GSE17891 | GEO

RNA-Seq Samples of siTFE3 in 8988T PDA Cell Line to Investigate Transcriptional Control of the Autophagy-Lysosome System

Project description:The activation of cellular quality control pathways to maintain metabolic homeostasis and mitigate diverse cellular stresses is emerging as a critical growth and survival mechanism in many cancers. Autophagy, a highly conserved cellular self-degradative process, is a key player in the initiation and maintenance of pancreatic ductal adenocarcinoma (PDA). However, the regulatory circuits that activate autophagy, and how they enable reprogramming of PDA cell metabolism are unknown. We now show that autophagy regulation in PDA occurs as part of a broader program that coordinates activation of lysosome biogenesis, function and nutrient scavenging, through constitutive activation of the MiT/TFE family of bHLH transcription factors. In PDA cells, the MiT/TFE proteins - MITF, TFE3 and TFEB - override a regulatory mechanism that controls their nuclear translocation, resulting in their constitutive activation. By orchestrating the expression of a coherent network of genes that induce high levels of lysosomal catabolic function, the MiT/TFE factors are required for proliferation and tumorigenicity of PDA cells. Importantly, unbiased global metabolite profiling reveals that MiT/TFE-dependent autophagy-lysosomal activation is specifically required to maintain intracellular AA pools in PDA. This AA flux is part of a program that is essential for metabolic homeostasis and bioenergetics of PDA but not for their non-transformed counterparts. These results identify the MiT/TFE transcription factors as master regulators of the autophagy-lysosomal system in PDA and demonstrate a central role of the autophagosome-lysosome compartment in maintaining tumor cell metabolism through alternative amino acid acquisition and utilization. Examination of mRNA levels in pancreatic ductal adenocarcinoma (PDA) cell line 8988T after treatment with siRNA for control or TFE3

2015-04-03 | E-GEOD-62077 | biostudies-arrayexpress

In vivo co-transplant gene expression

Project description:Gene expression of bulk subcutaneous tumors growing from either KPC PDA tumor cells co-transplanted with CD105pos Pancreatic Fibroblasts (PaFs) or CD105neg PaFs

2021-06-03 | GSE176056 | GEO

Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 in pancreas cancer

Project description:An autochthonous model of pancreatic ductal adenocarcinoma (PDA) permitted the analysis of why immunotherapy is ineffective in this human disease. Despite finding that PDA-bearing mice had cancer cell-specific CD8+ T cells, the mice, like human PDA patients, did not respond to two immunological checkpoint antagonists that promote the function of T cells, α-CTLA-4 and α-PD-L1. Immune control of PDA growth was achieved, however, by depleting carcinoma-associated fibroblasts (CAFs) that express Fibroblast Activation Protein (FAP). The depletion of the FAP+ stromal cell also uncovered the anti-tumor effects of α-CTLA-4 and α-PD-L1, indicating that its immune suppressive activity accounts for the failure of these T cell checkpoint antagonists. Three findings suggested that CXCL12 explained the overriding immunosuppression by the FAP+ cell: T cells were absent from regions of the tumor containing cancer cells; cancer cells were coated with the chemokine, CXCL12; and the FAP+ CAF was the principle source of CXCL12 in the tumor. Administering AMD3100, a CXCL12 receptor (CXCR4) inhibitor, induced rapid T cell accumulation among cancer cells, and acted synergistically with α-PD-L1 to selectively and greatly diminish cancer cells, identified by their loss-of-heterozygosity (LOH) of Trp53. The residual tumor was comprised only of pre-malignant epithelial cells and inflammatory cells. Thus, a single protein, CXCL12, from a single stromal cell type, the FAP+ CAF, may direct tumor immune evasion in a model of human PDA.

2012-11-30 | GSE42605 | GEO

Penicillium brasilianum cultivated on PDA and PDA control

Project description:extract from Penicillium brasilianum cultivated on PDA

2021-07-27 | MSV000087890 | MassIVE

PDA Indolylmaleimides Induce Anti-Tumor Effects in Prostate Carcinoma Cell Lines through Mitotic Death

Project description:Introduction: Castrate resistant prostate cancer in men shares several characteristics with late-stage canine prostate cancer. Consequently, dogs became a model organism for the study of the human disease. Due to current insufficient therapies, evaluation of novel therapeutic agents for late-stage prostate cancer is of considerable interest for both species. Methods: In this interdisciplinary study we characterized the influence of two indolylmaleimides (PDA-66 and PDA-377) on human and canine prostate carcinoma cell lines. For this purpose, we analyzed morphology, proliferation and apoptosis, recorded live cell imaging movies and performed whole transcriptome sequencing. Results: While PDA-377 showed only weak growth inhibition on the human prostate cancer cell lines, PDA-66 inhibited proliferation and induced apoptosis in all prostate carcinoma cell lines with concentrations in the low micromolar range. Morphological characterization and whole transcriptome sequencing revealed that PDA-66 induces mitotic death through its microtubule-depolymerizing ability. Discussion: PDA-66 appears to be a worthwhile anti-mitotic agent for further evaluation. The similarities in cellular and molecular response observed in the cell lines of both origins form a solid basis for the use of canine PCa in vivo models to provide valuable transferable findings to the benefit of both species.

2021-01-12 | GSE162832 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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