Combined VEGFR and MAPK pathway inhibition in angiosarcoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA693791 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Combined inhibition of the VEGF and MAPK pathways with cediranib and trametinib had an additive effect in in vitro models, and a combinatorial effect in an in vivo model. Combined treatment led to smaller tumors than treatment with either agent alone. RNA-seq demonstrated distinct expression signatures between the trametinib treated tumors and those treated with both trametinib and cediranib.
2022-01-19 | GSE165234 | GEO
Project description: Not available
| S-EPMC8087824 | biostudies-literature
Project description:A comparison of gene expression in OCT frozen human angiosarcoma compared with OCT frozen normal mesenchymal tissues
2013-10-21 | GSE44115 | GEO
Project description:Angiosarcoma is an aggressive soft-tissue sarcoma with a poor prognosis. Chemotherapy for this cancer typically employs paclitaxel, one of the taxanes (genotoxic drugs), although it has a limited effect due to chemoresistance for prolonged treatment. Here we examine a new angiosarcoma treatment approach that combines chemotherapeutic and senolytic agents. We first find that the chemotherapeutic drugs, cisplatin and paclitaxel, efficiently induce cellular senescence of angiosarcoma cells. Subsequent treatment with a senolytic agent, ABT-263, eliminates senescent cells through the activation of the apoptotic pathway. In addition, expression analysis indicates that senescence-associated secretory phenotype (SASP) genes are activated in senescent angiosarcoma cells and that ABT-263 treatment eliminates senescent cells expressing genes in the type-I interferon (IFN-I) pathway. Moreover, we show that cisplatin treatment alone requires a high dose to remove angiosarcoma cells, whereas a lower dose of cisplatin is sufficient to induce senescence, followed by the elimination of senescent cells by senolytic treatment. This study sheds light on a potential therapeutic strategy against angiosarcoma by combining a relatively low dose of cisplatin with the ABT-263 senolytic agent, which can help ease the deleterious side effects of chemotherapy.
2024-03-23 | GSE245935 | GEO
Project description:Gene expression profiling of human angiosarcoma samples was performed using the NanoString Human nCounter PanCancer IO 360 Panel
2023-05-03 | GSE226338 | GEO
Project description:Analysis of the effects of 4 hr and 24 hr propranolol treatment on gene expression of SVR mouse angiosarcoma cells. The hypothesis tested in the present study was that inhibiton of beta adrenergic receptor signaling could ablate the oncogenic properties of angiosarcoma cells. Results provide important information of the response of angiosarcoma cells to ablated beta adrenergic receptor signaling.
2013-06-01 | GSE42534 | GEO
Project description:Analysis of the effects of 4 hr and 24 hr propranolol treatment on gene expression of SVR mouse angiosarcoma cells. The hypothesis tested in the present study was that inhibiton of beta adrenergic receptor signaling could ablate the oncogenic properties of angiosarcoma cells. Results provide important information of the response of angiosarcoma cells to ablated beta adrenergic receptor signaling. The total RNA was obtained from mouse angiosarcoma cells cultured in monolayer at 0, 4, and 24 hrs of 50 micromolar propranolol treatment. Illumina microarrays were performed to determine the whole genome expression changes following treatment.
2013-06-01 | E-GEOD-42534 | biostudies-arrayexpress
Project description:A comparison of gene expression in OCT frozen human angiosarcoma compared with OCT frozen normal mesenchymal tissues RNA was isolated from 18 AS and normal human. RNA was isolated from 3 kidney and 2 skeletal muscle OCT frozen sections and 3 samples of frozen whole blood. Twenty-five nanograms of total RNA from each sample was used for amplification, and then was fluorescently labeled using Cy3 and hybridized onto Agilent whole human genome 8x60k gene expression microarrays (Agilent Technologies, Santa Clara, CA) according to Agilent standard procedures. After hybridization for 17 h at 65 oC and 10 rpm, the arrays were washed and scanned with the Agilent G3 high-resolution scanner. Probe features were extracted from the microarray scan data using Feature Extraction software v.10.7.3.1 (Agilent Technologies). Microarray data was read and processed with R/Bioconductor (version 2.15.1/2.16) statistical software environment using the limma package (version 3.12.1). The raw data was within array quantile normalized and probes that mapped to the same gene were combined by averaging.
2013-10-21 | E-GEOD-44115 | biostudies-arrayexpress
Project description:Developing strategies to overcome the frequent resistance to VEGF/VEGFR inhibitors in patients is a major challenge in antiangiogenic therapy for cancer. Targeting the VEGF pathway in vivo induces hypoxia and therefore enables to study drug-induced hypoxia in tumors. Hypoxia also occurs in the spontaneous evolution of cancers, particularly around areas of necrosis. Using cell markers such as CD133, CXCR4, or ALDH1, we identified stem-like cells in peri-necrotic areas in human biopsies and xenografts models of renal cancers. These stem-like cells were able in vitro to self-renew, form carcinoma spheres and had a tumorigenic potency, thus showing characteristics of stem-like cancer cells. In xenografted human renal cell carcinoma, we further demonstrated a strong link between necrosis, either spontaneous or treatment-induced, and the presence of CD133/CXCR4 double positive stem-like cells. Hypoxia increased their tumorigenic potency, induced overexpression of metallothionein2A, which we here identified as critical regulator of resistance to VEGFR-inhibition.
2014-12-31 | GSE32414 | GEO
Project description:We have used a chimeric VEGFR-2 in which the extracellular domain of mouse VEGFR-2 was replaced with the extracellular domain of human CSF-1 receptor. VEGFR-2 was immunoprecipitated with anti-VEGFR-2 antibody from PAE cells ectopically expressing VEGFR-2. The immunoprecipitated proteins were eluted and separated on SDS-PAGE, followed by in-gel chymotrypsin or trypsin digestion. The digested samples were analyzed by nano LC/MS/MS on a Thermo Fisher LTQ Orbitrap XL. The LC-MS/MS data were analyzed using Proteome Discoverer (Thermo Fisher Scientific; Version 1.3.0.339). MS/MS search was carried out using Sequest search algorithm against the sequence of target mouse protein from the UniProtKB database. Search parameters included chymotrypsin as the enzyme with four missed cleavage allowed; methylation at lysine and arginine, phosphorylation of serine, threonine, and tyrosine, alkylation at cysteine, and oxidation of methionine were set as dynamic modifications. Precursor and fragment mass tolerance were set to 5 ppm and 0.8 Da, respectively. The false discovery rate was calculated by enabling the peptide sequence analysis using a decoy database. High confidence peptide identifications were obtained by setting a target false discovery rate threshold of 1% at the peptide level.
2019-11-22 | PXD000520 | Pride