Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse liver from tumor bearing animals by TSU68 treatment

ABSTRACT: The aim of this study was to investigate the inhibitory effect of TSU68, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor beta (PDGFRÎ²) and fibroblast growth factor receptor 1 (FGFR1), on colon cancer liver metastasis and to test the hypothesis that TSU68 modulates the microenvironment in the liver before the formation of metastasis. Experiment Overall Design: The human colon cancer TK-4 was implanted orthotopically into cecal walls of 6-week-old male BALB/c nu/nu mice (Clea Japan, Tokyo, Japan). The animals were treated with TSU68 (400 mg/kg/day, twice-daily, p.o.) or vehicle from 7 days after orthotopic implantation. After one week of drug administration, livers were removed and total RNA was extracted. Experiment Overall Design: We established four different groups of mice; non-tumor-bearing and treated with vehicle alone (NT-Co), non-tumor-bearing and treated with TSU68 (NT-TSU), tumor-bearing and treated with vehicle (T-Co), and tumor-bearing and treated with TSU68 (T-TSU). NT-Co, T-Co and T-TSU group were applied to microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: M Yamamoto

PROVIDER: E-GEOD-11808 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [nude mice]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 Nu/Nu mice Tumor-bearing bone marrows of three Sca1-TOMATO-Lmo2 Nu/Nu mice compared with bone marrow cells from four Control Nude mice and with thymus leukemic cells from ten Sca1-TOMATO-Lmo2 mice. GSM2209767 - GSM2209776 are re-analyses of GSE83570 (GSM2209749 - GSM220975 and GSM2209757 - GSM2209759).

2016-06-22 | E-GEOD-83571 | biostudies-arrayexpress

LMO2 expression in HSCs causes T-ALL in the presence of an intact thymic niche [nude mice]

Project description:We used microarrays to investigate gene expression changes in tumor-bearing Sca1-TOMATO-Lmo2 Nu/Nu mice

2016-06-22 | GSE83571 | GEO

RAW264.7 cells: RANKL vs Bone Metastasis Tumor Cell Condidtioned Media

Project description:Transcriptional profiling of differential miRNA expression in mouse RAW264.7 preosteoclast cells comparing control untreated cells with RAW264.7 cells treated for 6 days. Treatment conditiones tested included 50ng/mL RANKL or indicated bone metastasis tumor cell conditioned media from 4T1, 4T1.2, TSU-PR1, and TSU-PR1-B2 cell lines.

2013-10-14 | GSE44936 | GEO

Gene expression profiling of HhAntag-treated pancreatic xenografts

Project description:Four vehicle-treated and four HhAntag-treated pancreatic xenograft tumors were profiled for gene expression changes using Affymetrix U133 Plus 2.0 and Affymetrix Mouse Genome 430 2.0 arrays. Keywords: comparative gene expression, hedgehog, hh A primary human pancreatic tumor xenograft (1051178-A) was established by direct implantation of surgical material into female CD1 nu/nu mice of 6-8 weeks of age. Tumors were serially passaged into larger cohorts of mice for efficacy testing and subsequently distributed into tumor volume-matched cohorts upon tumors reaching between 200 to 350 mm3. HhAntag was resuspended in 0.5% methyl-cellulose, 0.2% Tween-80 (MCT) and administered orally twice daily at 75 mg/kg from a 10 mg/ml suspension. MCT alone served as vehicle control. Tumor xenografts (4/group) were excised following 21 days of dosing and RNA was extracted. Preparation of complementary RNA, Human Genome U133 Plus 2.0 array and Mouse Genome 430 2.0 array hybridizations, and subsequent data analysis were carried out using Affymetrix protocols, with signal intensities being determined by the MAS5.0 algorithm.

2008-09-12 | E-GEOD-11981 | biostudies-arrayexpress

Orthotopic KI tumors treated with vehicle or IRAK4 inhibitor CA-4948 for two weeks

Project description:We treated FVBN/J mice bearing orthotopic KI tumors with vehicle or CA-4948 for two weeks and performed bulk RNASeq to assess transcriptomic changes in the tumor

2022-12-31 | GSE197328 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes

Project description:Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) between tumors of mammary tumor bearing mice treated with a vehicle control or FDA approved Hedgehog signaling inhibitor, Vismodegib.

2023-02-01 | GSE146222 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes II

2021-11-10 | GSE171168 | GEO

RAW264.7 cells: RANKL vs Bone Metastasis Tumor Cell Condidtioned Media

2013-10-14 | E-GEOD-44936 | biostudies-arrayexpress

Effect of Sunitinib treatment withdrawal on Immunodeficient mice bearing MDA-MB231 tumors

Project description:Immunodeficient RAG1-/- mice bearing MDA-MB231-LUC+ tumors of 50-70 mm3 were daily administrated by gavage with vehicle (containing, 0.5% carboxymethylcellulose, 1.8 % NaCl, 0.4 % Tween-80, 0.9 %. benzyl alcohol, and ultrapure water adjusted to pH 6.0) or sunitinib (40mg/kg/day) for 30 days followed by treatment withdrawal for 3-4 weeks to allow the tumor regrowth until reaching the same volume as that of the vehicle treated group. Mice were sacrificed when tumor reached the volume of 350-400 mm3 and RNAs of two tumors from two different mice treated with sunitinib or vehicle were extracted.

2014-08-24 | GSE50795 | GEO

TWEAK-treated time course in CAKI cells grown as xenografts

Project description:Tumor necrosis factor-related weak inducer of apoptosis, TWEAK, is a TNF superfamily member that mediates signaling through its receptor fibroblast growth factor inducible-14, Fn14. In tumor cell lines, TWEAK induces proliferation, survival and NF-kappaB signaling and gene expression that promote tumor growth and suppress antitumor immune responses. Anti-TWEAK antibody, RG7212, inhibits tumor growth in vivo with decreases in pathway activation markers and modulation of tumor, blood and spleen immune cell composition. Candidate response prediction markers, including Fn14, have been identified in mouse models. Phase I pharmacodynamic data from patients are consistent with preclinical results. TWEAK:Fn14 signaling is upregulated in human cancer and pathway activation induces tumor proliferation and survival signaling. Blockade with anti-TWEAK mAb, RG7212, inhibits tumor growth in multiple models in mice. TWEAK induces changes that suppress anti-tumor immune responses and RG7212 blocks these effects resulting in changes in tumor immune cell composition and decreases in cytokines that promote immunosuppression. Antitumor efficacy in mice was observed in a range of Fn14 expressing models with pathway activation and expressing either wild-type or mutant p53, BRAF or KRAS suggesting both a patient selection strategy and potential broad clinical applicability. Preclinical mechanism of action hypotheses are supported by Phase I clinical data, with decreases in proliferation markers and increased tumor T cell infiltration. CAKI cells impanted as xenografts in Athymic, Nu/Nu nude mice, treated with anti-TWEAK antibody (TW212) or Vehicle for 24 hours. Four replicates for each condition were performed. RNA was extracted from xenografts, processed and hybridized to human and mouse chips.

2013-10-04 | E-GEOD-42049 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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