Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics of Mouse Syngeneic Models

ABSTRACT: The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Lung Cancer,Colon Cancer,Kidney Cancer,Breast Cancer

SUBMITTER: Jeremy Myers

LAB HEAD: Jeremy S. Myers

PROVIDER: PXD011885 | Pride | 2019-12-03

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	1015_Balb-c-1-mem_Q-E_r1.raw	Raw
	1015_Balb-c-1-mem_Q-E_r2.raw	Raw
	1015_Balb-c-2-mem_Q-E_r1.raw	Raw
	1015_Balb-c-2-mem_Q-E_r2.raw	Raw
	1015_C57-BL6-1-mem_Q-E_r1.raw	Raw

Items per page:

1 - 5 of 141

Similar Datasets

RNASeq analysis of Myeloid Derived Suppressor Cells (MDSCs) from MC38 syngeneic mice to study their role on tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

Project description:Understanding MoA of ceralasertib (AZD6738) in driving efficacy through immune regulation via polymorphonuclear-myeloid derived suppressor cells (PMN-MDSC) and monocytic-myeloid derived suppressor cells (M-MDSC) on tumour intrinsic pathways (STING/IFN) for AZD6738 driven efficacy. Animals were treated only for 7 days and left for further 7 days without treatment. We compared cells against Vehicle and spleen derived ( naive) as a positive control.

2024-01-30 | E-MTAB-13707 | biostudies-arrayexpress

Transcriptomic analysis by array of reactivation of dihydroorotate dehydrogenase by respiration restores tumor growth of mitochondrial DNA-depleted cancer cells.

Project description:Tumor cells without mitochondrial DNA (mtDNA) reconstitute oxidative phosphorylation (OXPHOS) by acquiring host mitochondria from stromal cells, but the reasons why functional respiration is crucial for tumorigenesis remain unclear. To address this issue, we used time-resolved analysis of the initial stages of tumor formation by cells devoid of mtDNA and genetic manipulations of components of OXPHOS. We show that pyrimidine biosynthesis, supported by respiration-linked dihydroorotate dehydrogenase (DHODH), is strictly required to overcome cell cycle arrest, while mitochondrial ATP generation is dispensable for tumorigenesis.

2018-10-01 | E-MTAB-6150 | biostudies-arrayexpress

the profile of iPSC cell membrane

Project description:Analysis of significantly upregulated proteins shared by tumor cell membrane and iPSC cell membrane compared to MEF membrane.

2024-10-10 | PXD056678 | Pride

Gene expression analysis of 4T1 tumors expressing mouse urokinase plasminogen activitor (uPA)

Project description:Analysis of uPA regulation of 4T1 tumor growth at gene expression level. The hypothesis tested in the present study was that overexpression of uPA in 4T1 tumor influence the tumor growth and metastasis related cell signaling pathway. 4T1 cells were stably transduced by lentiviral vector expressing mouse uPA or empty vector. After day 7 of inoculation of 4T1 cells into fatpad of Balb/c mice. Total RNA was extracted from tumor samples (triplicate) using Qiagen total RNA isolation kit. The Illumina MouseWG-6 v2.0 Expression BeadChip (Illumina, Wallingford, CT) was used for gene expression. The raw data from the fluorescence intensity measurements of each array experiment was processed using GeneSpringGX v.11.0 software (Agilent, Santa Clara, CA). Statistical analysis, fold change calculations, and hierarchical clustering of the data were also performed in GeneSpring software. Genes that expressed significantly differently with more than 1.5-fold change and a p-value of <0.05 with respect to controls were taken into consideration. Gene expression data were further validated by qRT-PCR analysis. Pathway analysis was performed by MetaCore software (GeneGo, Inc, St. Joseph, MI).

2012-05-30 | E-GEOD-38346 | biostudies-arrayexpress

Mouse cytokine antibody array

Project description:Tumors of hematopoietic stem cell transplantation (HSCT) or control mice were collected at day 14 post transplantation. Comprehensive analysis of cytokine levels were performed by using commercially available RayBio Mouse Cytokine Array G series III and IV (RayBiotech, Inc.) according to manufacturerM-^As protocol. There are two samples: non-HSCT control group and HSCT group. Each group consists of 2 replications.

2013-08-28 | E-MTAB-1761 | biostudies-arrayexpress

4T1 RNA-Seq

Project description:Background: the transcription of tumor mutations from DNA into RNA has implications for biology, epigenetics and clinical practice. It is not clear if mutations are in general transcribed and, if so, at what proportion to the wild-type allele. Here, we examined the correlation between DNA mutation allele frequency and RNA mutation allele frequency. Methods: we sequenced the exome and transcriptome of tumor cell lines with large copy number variations, identified heterozygous single nucleotide mutations and absolute DNA copy number, and determined the corresponding DNA and RNA mutation allele fraction. Results: we found that 99% of the DNA mutations in expressed genes are expressed as RNA. Moreover, we found a high correlation between the DNA and RNA mutation allele frequency. Exceptions are mutations that cause premature termination codons and therefore activate nonsense-mediated decay. Beyond this, we did not find evidence of any wide-scale mechanism, such as allele-specific epigenetic silencing, preferentially promoting mutated or wild-type alleles. Conclusion: taken together, our data strongly suggest that genes are equally transcribed from all alleles, mutated and wild-type, and thus transcribed in proportion to their DNA allele frequency.

2014-03-05 | E-MTAB-2383 | biostudies-arrayexpress

RNA-seq of CT26 subcutaneous tumors expressing control or Gna13 targeting sgRNAs

Project description:CT26 cells expressing lentiviral Cas9 and sgRNAs targeting either control or Gna13 were transplanted into immunocompetent BALB/c mice. Tumors were harvested and processed for RNA-seq

2021-10-01 | E-MTAB-10737 | biostudies-arrayexpress

RNAseq profiling of tumor, tumor-draining-lymph nodes, blood and tumor-associated macrophages of MC38 mice treated with the PI3Kg inhibitor AZD3458 and a combination of AZD3458 and anti-PD-1

Project description:RNAseq profiling of AZD3458 monotherapy and combination treatment with anti-PD-1 of whole tumors, isolated tumor macrophages (Mac) (CD45+CD11b+F4/80+), whole blood (PB) and tumor draining lymph nodes (TDLN) were assessed to elucidate further mechanisms leading to enhanced combination activity.

2021-02-28 | E-MTAB-10057 | biostudies-arrayexpress

17β-estradiol accelerates ovarian tumour progression in vivo though the upregulation of GREB1

Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2. Three biological replicates (MASE2 tumours grown in SCID mice, see growth protocol) were analyzed for both conditions of addition of E2 or placebo.

2014-01-20 | E-GEOD-45271 | biostudies-arrayexpress

RNASeq analysis of solid tumours from CT26 syngeneic mice to study the role of T-cells and tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

Project description:Understanding MoA of ceralasertib (AZD6738) in driving efficacy through immune regulation via T-cells and tumour intrinsic pathways (STING/IFN) for AZD6738 driven efficacy.

2024-01-29 | E-MTAB-13703 | 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