Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell transcriptomic of murine pancreatic tumor model by treatment of PD-L1-directed PlGF/VEGF blockade

ABSTRACT: We developed a multi-paratopic VEGF decoy receptor (Ate-Grab) by fusing the scFv of atezolizumab to VEGF-Grab to target PD-L1 expressing cells in tumor microenvironment. We compared the single-cell transcriptomes of gemcitabine-treated and Ate-Grab with Gemcitabine-treated Pan02 tumors. We confirmed the subtype of cancer-associated fibroblasts(CAFs) that modulates the collagen inside the tumor microenvrionment. In the Ate-Grab+Gemcitabine group, it was confirmed that new CAFs were regulated.

ORGANISM(S): Mus musculus

PROVIDER: GSE189753 | GEO | 2022/09/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from gemcitabine treated pancreatic CAFs

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naÃ¯ve CAFs (N-CAFs) and R-CAFs were compared by array analysis. Immortalized human pancreatic CAFs were grown for 30 days in either control media or media containing 100nM gemcitabine. RNA was then isolated and hybidized on U133 Plus 2.0 Affymetrix arrays.

2016-03-09 | E-GEOD-78982 | biostudies-arrayexpress

Immunomodulatory effect of cisplatin and carboplatin in human and mouse cell line in vitro

Project description:The Phase 3 1L urothelial carcinoma (IMvigor130) trial revealed more favorable effects on overall survival with atezolizumab combined with gemcitabine and cisplatin (GemCis) than with atezolizumab combined with gemcitabine and carboplatin (GemCarbo). This study investigates the immunomodulatory effects of cisplatin vs carboplatin as a potential explanation for these clinical observations. GemCis compared with GemCarbo ± atezolizumab induced transcriptional changes in circulating immune cells, including upregulation of antigen presentation and T-cell activation programs. In vitro experiments demonstrated that cisplatin, compared with carboplatin, exerted direct immunomodulatory effects on cancer cells, promoting dendritic cell activation and antigen-specific T cell killing. These results underscore the key role of immune modulation in cisplatin's efficacy in urothelial carcinoma and highlight the potential importance of specific chemotherapy backbones for immune checkpoint blockade combination therapies.

2023-11-02 | GSE235066 | GEO

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

Project description:We asked whether combining Notch and VEGF blockade would enhance suppression of tumor angiogenesis and growth, using the NGP neuroblastoma model. NGP tumors were engineered to express a Notch1 decoy construct (N1D), which restricts Notch signaling, and then treated with either the anti-VEGF antibody bevacizumab or vehicle. Combining Notch and VEGF blockade led to blood vessel regression, increasing endothelial cell apoptosis and disrupting pericyte coverage of endothelial cells. Combined Notch and VEGF blockade did not affect tumor weight, but did additively reduce tumor viability. Our results indicate that Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis, and show that concurrent blockade disrupts primary tumor vasculature and viability further than inhibition of either pathway alone. 6 neuroblastoma tumors were transfected with Notch1 decoy, 6 with Notch1 decoy and treated with bevacizumab, 6 tumors treated with bevacizumab, and 6 control tumors were profiled by human 133A 2.0 arrays

2013-12-01 | E-GEOD-48880 | biostudies-arrayexpress

Expression data from gemcitabine treated pancreatic CAFs

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a characteristically dense stroma comprised predominantly of cancer associated fibroblasts (CAFs). CAFs promote tumor growth, metastasis and treatment resistance. We aimed to investigate the molecular changes and functional consequences associated with chemotherapy treatment of PDAC CAFs. Chemoresistant immortalized CAFs (R-CAFs) were generated by continuous incubation in 100nM gemcitabine. Gene expression differences between treatment naïve CAFs (N-CAFs) and R-CAFs were compared by array analysis.

2016-03-09 | GSE78982 | GEO

Homo sapiens

Project description:Expression data from gemcitabine treated pancreatic CAFs

| PRJNA314574 | ENA

MicroRNAs upregulated in cancer associated fibroblasts following gemctiabine treatment

Project description:Cancer associated fibroblasts (CAFs) comprise the majority of the tumor bulk of pancreatic adenocarcinomas (PDACs). Current efforts to eradicate these tumors focus predominantly on targeting the proliferation of rapidly growing cancer epithelial cells. We know that this is largely ineffective with resistance arising in most tumors following exposure to chemotherapy. Despite the long-standing recognition of the prominence of CAFs in PDAC, the effect of chemotherapy on CAFs and how they may contribute to drug resistance in neighboring cancer cells is not well characterized. Here we show that CAFs exposed to chemotherapy play an active role in regulating the survival and proliferation of cancer cells. We found that CAFs are intrinsically resistant to gemcitabine, the chemotherapeutic standard of care for PDAC. Further, CAFs exposed to gemcitabine significantly increase the release of extracellular vesicles called exosomes. These exosomes increased chemoresistance-inducing factor, Snail, in recipient epithelial cells and promote proliferation and drug resistance. Finally, treatment of gemcitabine-exposed CAFs with an inhibitor of exosome release, GW4869, significantly reduces survival in co-cultured epithelial cells, signifying an important role of CAF exosomes in chemotherapeutic drug resistance. Collectively, these findings show the potential for exosome inhibitors as treatment options alongside chemotherapy for overcoming PDAC chemoresistance.

2016-11-01 | GSE85048 | GEO

Transcriptome profiling by array of normal fibroblasts and cancer associated fibroblasts (CAF) isolated from breast cancer skin metastasis, cutaneous basal cell carcinoma and squamous cell carcinoma arising from oral cavity mucous membrane

Project description:We focus on cancer-associated fibroblasts (CAFs) as an active component of the tumor microenvironment. The transcriptome profiling and analysis of CAFs isolated from breast cancer skin metastasis, cutaneous basal cell carcinoma and squamous cell carcinoma arising from oral cavity mucous membrane unravelled major gene candidates such as the IL-6, VEGF-A and MFGE8 that induced the expression of several markers associated with poor prognosis and epithelial-to-mesenchymal transition in co-cultivated EM-G3 breast cancer cells.

2023-10-02 | E-MTAB-12994 | biostudies-arrayexpress

Notch and VEGF pathways play distinct but complementary roles in tumor angiogenesis

2013-12-01 | GSE48880 | GEO

Hypoxia-induced proteomic remodeling of human mammary cancer associated fibroblast - siRNA NCBP2-AS2

Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Amongst those, the uncharacterized antisense gene protein NCBP2-AS2 is one of the most transcriptionally upregulated proteins in the proteome and secretome of hypoxic CAFs. Silencing of NCBP2-AS2 abrogates the pro-angiogenic function acquired by hypoxic CAFs through decreasing VEGF expression levels to the levels found in normoxic CAFs.

2019-02-15 | PXD006539 | Pride

PlGF and IL6 effect on CD3/CD28-stimulated mouse splenic CD4+ T cell

Project description:T-helper (Th) cells actively communicate with adjacent cells by secreting soluble mediators, and yet crosstalk between Th cells and endothelial cells is poorly understood. Placental growth factor (PlGF), originally identified in the placenta, is an angiogenic factor homologous to vascular endothelial growth factor (VEGF)-A. We performed transcriptome analysis to systemically compare the effect of IL6, a key factor in Th cell polarization, and PlGF on T cell functions.

2019-06-14 | GSE118281 | 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