Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of mouse ovarian cancer treated with anti-VEGF antibody

ABSTRACT: Ovarian cancer is a highly aggressive female tract cancer. Anti-VEGF therapy is widely used for the treatment of ovarian cancer, however it has shown moderate impact on patient prognosis. The elucidation of mechanism of drug resistance is highly beneficial for the advances in ovarian cancer treatment. Here, we investigated gene expression profile of HM-1 tumor which were treated with or without anti-VEGF antibody (B20-4.1.1) using transcriptome array to identify special molecular features of ovarian tumor after anti-VEGF treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE115944 | GEO | 2018/06/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of anti-human VEGF-treated tumor xenografts formed by IGROV-1 or SKOV3 cells

Project description:This microarray experiment was designed to identify genes and pathways modulated in ovarian cancer xenografts treated with anti-human VEGF mAb (Bevacizumab). Tumors were established in NOD/SCID mice by s.c. injection of human ovarian cancer cells (IGROV-1 and SKOV3). Mice were treated with the anti-VEGF monoclonal antibody Bevacizumab or with PBS (control). Total RNA was extracted from tumor samples and hybridized on Affymetrix GeneChip™ PrimeView™ Human Gene Expression Arrays. Each sample was derived from a different mouse (n=5 mice/group). In order to evaluate the effects of the anti-human VEGF mAb in the two models, expression data of IGROV-1 and SKOV3 derived tumors were normalized and analyzed separately. Raw microarray data, preprocessed data matrix and results of differential expression analysis are available together with the applied protocols.

2019-12-16 | E-MTAB-7683 | biostudies-arrayexpress

Gene expression analysis of mouse ovarian cancer treated with anti-VEGF antibody

Project description:Gene expression analysis of mouse ovarian cancer treated with anti-VEGF antibody

| PRJNA476570 | ENA

Gene expression data of MKN45 xenograft tumors treated with anti-VEGFR2 and anti-VEGF-A antibodies

Project description:The vascular endothelial growth factor (VEGF) /VEGF receptor (VEGFR) axis is an essential regulator of angiogenesis and important therapeutic target in cancer. However, the efficacy of combination treatment with an anti-VEGFR2 antibody and anti-VEGFR-A antibody on tumor progression is not clear. In this study, we examined the anti-tumor effect of the combination treatment using BALB/c-nu/nu mouse xenograft model subcutaneously injected with human gastric cancer MKN45 cells. In this model, we evaluated intra-tumor molecular changes after the combination treatment by cDNA microarray analysis.

2021-07-28 | GSE160613 | GEO

Extracellular vimentin mimics VEGF and is a target for anti-angiogenic immunotherapy

Project description:Anti-angiogenic anticancer therapies possess immune-stimulatory properties by counteracting pro-angiogenic molecular mechanisms. We report that tumor endothelial cells ubiquitously overexpress and secrete the intermediate filament protein vimentin through type III unconventional mechanisms. Extracellular vimentin is pro-angiogenic and functionally mimics VEGF action, while concomitantly acting as inhibitor of leukocyte-endothelial interactions. Targeting of extracellular vimentin presents a promising anti-angiogenic immunotherapy strategy against cancer. Here we describe profiling of the HUVEC (Human Umbilical Vein Endothelial Cell) proteome, with special emphasis on vimentin (variants) in the different fractions. We have evidence that vimentin is externalized and deposited in the matrix of cultured cells and is as such available for targeted antiangiogenic therapeutics. The aim of the experiment is to determine the protein variants of vimentin in the cell, the secretome, and in the matrix deposited by the cells.

2022-03-29 | PXD024426 | Pride

Fibroblasts associated with tumors refractory to anti-VEGF treatment

Project description:PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment Tumor associated fibroblasts (TAF) from different tumors exhibit distinct angiogenic and tumorigenic properties. Unlike normal skin fibroblasts (NSF) or TAF (TAF-TIB6) from TIB6 tumors that are sensitive to anti-VEGF treatment, TAF (TAF-EL4) from resistant EL4 tumors can stimulate TIB6 tumor growth even when VEGF is inhibited. We show that platelet-derived growth factor (PDGF)-C is upregulated in TAFs from resistant tumors. PDGF-C neutralizing antibodies blocked the angiogenesis induced by such TAF in vivo and slowed the growth of EL4 and admixture (TAF-EL4 + TIB6) tumors and exhibited additive effects with anti-VEGF-A antibodies. Hence, our data reveal a novel mechanism for TAF mediated tumorigenesis and suggest that some tumors may overcome inhibition of VEGF-mediated angiogenesis through upregulation of PDGF-C

2009-01-05 | GSE13549 | GEO

Expression data from mouse endothelial cell in human ovarian cancer

Project description:To examine potential mechanisms underlying resistance to anti-VEGF antibody (AVA) therapy, we used mouse models to identify tumors that demonstrated growth subsequent to a period of initial response. Specifically, we established orthotopic mouse models of ovarian cancer designed to develop adaptive resistance after treatment with an AVA. To examine potential mechanisms underlying resistance to anti-VEGF antibody (AVA) therapy, we used mouse models to identify tumors that demonstrated growth subsequent to a period of initial response. Specifically, we established orthotopic mouse models of ovarian cancer designed to develop adaptive resistance after treatment with an AVA.

2021-07-25 | GSE180687 | GEO

Ovarian cancer cell line response to Snail depletion

Project description:Analysis of mouse ovarian cancer cell line HM-1 transfected with shRNA targeting Snail, an EMT inducer. Anti-tumor immuty in state of EMT remains unclear. We focused on Snail, a major EMT inducer, and explored the influence of Snail on immune ivasion into ovarian tumors by generating Snail knockdown cell line. Elucidating the mechanisms of Snail-induced immune evasion will lead to the development of novel treatment strategies for tumor undergoing EMT.

2018-01-27 | GSE109688 | GEO

Transcription profiling of human VEGF-derived CD8+ T-cell epitope

Project description:The vascular endothelial growth factor A (VEGF) is involved in various physiological processes such as angiogenesis or wound healing but is also crucial in pathological events such as tumor growth. Thus, clinical anti-VEGF treatments have been developed which could already prove to have enormous beneficial effects for cancer patients. In this article we describe the first VEGF-derived CD8+ T-cell epitope. The natural HLA ligand SRFGGAVVR was identified by differential mass spectrometry in two primary renal cell carcinomas (RCC) and was significantly over-presented on both tumor tissues. SRFGGAVVR is derived from a cryptic translated region of VEGF presumably by initiation of translation at the non-classical start codon CUG499. SRFGGAVVR specific T-cells were generated in vitro using peptide loaded dendritic cells or artificial antigen presenting cells. They were identified by HLA tetramer analysis after in vitro stimulation. SRFGGAVVR specific CD8+ T-cells were fully functional T-effector cells, which were able to secrete IFN-gamma upon stimulation and killed tumor cells in vitro. Additionally, we have quantitatively analyzed VEGF mRNA and protein levels in RCC tumor and normal tissue samples by gene chip analysis, qRT-PCR, in situ hybridization, and bead based immuno assay. In the future, T-cells directed against VEGF as a tumor associated antigen may represent a possible way of combining peptide-based anti-VEGF immunotherapy with already existent anti-VEGF cancer therapies. Experiment Overall Design: Two clear cell renal cell carcinomas including autologous normal tissue were analyzed.

2008-06-15 | E-GEOD-8050 | biostudies-arrayexpress

B-catenin downregulates Dicer to promote ovarian cancer metastasis

Project description:Ovarian cancer is a nearly uniform lethal disease and its highly aggressive metastatic phenotype portends a poor prognosis. Lack of a well-controlled, relevant experimental model has been a major obstacle to identifying key molecules causing metastasis. Here we describe the creation of a new isogenic model of spontaneous human ovarian cancer metastasis exhibiting opposite phenotypes - highly metastatic (HM) and non-metastatic (NM) - both in vitro and in vivo. HM was unique in its ability to metastasize consistently to the peritoneum, mimicking the major dissemination route of human ovarian cancer. In contrast, NM failed to form detectable metastases although it was equally tumorigenic. Using comparative label-free quantitative LC-MS/MS, we identified b-catenin which we demonstrated for the first time a direct role in the pathogenesis of ovarian cancer metastasis. Our studies also revealed a previously unrecognized role of b-catenin in the downregulation of multiple microRNAs (miRNAs) through attenuating miRNA biogenesis by targeting Dicer, a key component of the microRNA processing machinery. One such downregulated miRNAs was miR-29s involved in epithelial-to-mesenchymal transition and subsequent stem cell traits. Silencing b-catenin or overexpressing Dicer or miR-29 mimics in HM significantly reduced the ability of these cells to migrate. B-catenin knockdown cells also failed to metastasize in an orthotopic model of ovarian cancer. Meta-analysis revealed an increase in CTNNB1 and a decrease in DICER1 expression levels in the high-risk group. These results uncover b-catenin as a critical player in promoting ovarian cancer aggressiveness and a new mechanism linking between b-catenin and miRNA downregulation underlying this process.

2017-07-03 | PXD006327 | Pride

Mouse retinal tissue study in VEGF-induced hyperpermeability.

Project description:The goal of the project is to identify novel therapeutic targets for retinal vascular hyperpermeability. Three condition (Control, VEGF, and Anti-VEGF) sample of mouse retinal tissues were extensively characterized by global proteome profiling.

2016-03-22 | PXD003656 | Pride

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