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

Gene expression profiling of tumor cells and M2 macrophages from WT mice and mice with deletion of integrin beta3 in macrophage lineage cells (b3KOM)

ABSTRACT: To better understand the impact of integrin beta3 signaling in myeloid cells on the tumor microenvironment, we compared the gene expression profiles of FACS isolated GFP+ PyMT-BO1 MFP tumor cells and also M2 TAMs (CD11b+Gr1-F4/80+CD206+) from tumor tissue of WT mice and b3ÎÎÎ mice. PyMT-BO1-GFP-Luc tumor cells (100,000) were injected into mammary fat pad (MFP) tissue from WT and b3KOM mice. PyMT-BO1-GFP-Luc cells and CD206hi tumor-associated macrophages (TAMs) were FACS-sorted from day 10 MFP tumor tissue. FACS-sorted cells directly used for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Katherine Weilbaecher

PROVIDER: E-GEOD-75882 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of tumor cells and M2 macrophages from WT mice and mice with deletion of integrin beta3 in macrophage lineage cells (b3KOM)

Project description:To better understand the impact of integrin beta3 signaling in myeloid cells on the tumor microenvironment, we compared the gene expression profiles of FACS isolated GFP+ PyMT-BO1 MFP tumor cells and also M2 TAMs (CD11b+Gr1-F4/80+CD206+) from tumor tissue of WT mice and b3ΚΟΜ mice.

2015-12-11 | GSE75882 | GEO

An Ets2-specific transcriptional program in tumor-associated macrophages promotes metastasis

Project description:Macrophages have been implicated in breast cancer progression and metastasis, but relatively little is known about the genes and pathways that are involved. Using a conditional allele of Ets2 in the mouse, we have identified Ets2 as a critical gene in tumor associated macrophages (TAMs) that specifically promotes mammary tumor metastasis. Loss of Ets2 in TAMs decreased the frequency and size of lung metastases without impacting primary tumor burden. Expression profiling of isolated tumor macrophages established that Ets2 deficiency resulted in the de-repression of a defined set of anti-angiogenic genes. Activation of this transcriptional program correlated with decreased angiogenesis in metastatic tumors and decreased metastatic growth. Comparison of this Ets2-specific TAM expression profile with human breast cancer profiles revealed a macrophage gene expression signature that could predict overall survival of estrogen receptor negative patients. In summary, we have identified a critical factor, Ets2, in TAMs that represses a transcriptional program to promote the growth of mammary tumor metastases in the lung. Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling.

2010-01-05 | E-GEOD-12863 | biostudies-arrayexpress

Expression data from PyMT;Lys Cre:E2f3 f/f TAMs

Project description:To understand the underlying cause for reduced lung metastasis, we compared global gene expression profiles of F4/80+ FACS sorted tumor-associated macrophages (TAMs) PyMT;E2f3 f/f (control) and PyMT;Lys Cre:E2f3 f/f (experimental) mice. We compared gene expression profile between TAMs isolated from mammary tumors of PyMT;E2f3 f/f and PyMT;Lys Cre:E2f3 f/f mice

2017-04-04 | GSE67081 | GEO

RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

Project description:IL-15 is recognized as a promising candidate for tumor immunotherapy and has been described as both a promoter of cancer and a promoter of anti-cancer immunity. IL-15 was discovered in cells transformed by HTLV-1, the etiologic agent of adult T cell leukemia / lymphoma (ATL) and the human retrovirus that carries the Tax oncogene. We have developed the TAX-LUC mouse model of ATL in which Tax expression drives both malignant transformation and luciferase expression, enabling non-invasive imaging of tumorigenesis in real time. To identify the role of IL-15 in spontaneous development of lymphoma in vivo, an IL-15-/- TAX-LUC strain was developed and examined. The absence of IL-15 resulted in aggressive tumor growth and accelerated mortality and demonstrated that IL-15 was not required for Tax-mediated lymphoma but was essential for anti-tumor immunity. Further analysis revealed a unique transcriptional profile in tumor cells that arise in the absence of IL-15 that included a significant increase in the expression of IL-1α and IL-1α-regulated cytokines. Moreover, anti-IL-1α antibodies and an IL-1 receptor antagonist (Anakinra) were used to interrogate the potential of IL-1α targeted therapies in this model. Taken together, these findings identify IL-15 and IL-1α as therapeutic targets in lymphoma. We used microarrays to compare the gene expression profile of tumors in IL-15-/- TAX-LUC mice to IL-15+/+ TAX-LUC mice RNA was obtained from CD16/32HI and CD16/32LO cells harvested from n=2 IL-15+/+ (control)and n=2 IL-15-/- Tax tumors and was compared to look for alterations in gene expression in malignant and tumor infiltrating cells resulting from loss of IL-15 in vivo

2013-06-11 | E-GEOD-46072 | biostudies-arrayexpress

Expression data of Sox9+ and Ngn3+ mouse pancreas cells at different stages of development

Project description:Genes specific to Sox9+ pancreatic progenitors were identified by comparing the gene expression in embryonic and adult Sox9+ cells. We used microarray analysis to detail the global changes in gene expression as Sox9 positive embryonic pancreatic progenitors differentiatiate into adult ductal cells or the endocrine lineage. GFP positive cells from Sox9-EGFP mouse pancreas were isolated by FACS at different stages of development (e10.5, e15.5, and p23) for RNA extraction and hybridization to Affymetrix microarrays. To obtain populations highly enriched in Sox9 expression, we collected only GFP Hi populations for analysis. To identify gene expression changes specific to the differentiation of progenitors to ductal cells or endocrine cells, we also isolated and analyzed the gene expression profile of GFP negative cells isolated at p23, as well as GFP positive cells isolated from Ngn3-EGFP mouse pancreas at e15.5. These two populations allow the identification of genes whose expression is associated with the newly differentiated endocrine progeny in the embryo (Ngn3-GFP positive) and adult acinar and endocrine cells at p23.

2012-08-01 | E-GEOD-34060 | biostudies-arrayexpress

Gene expression profile at single nucleus level for tumor associated macrophage (TAMs) nuclei sorted from tumor of control-PyMT and S100a8-creRosa26-LSL-MYCPyMT (MYC-PyMT) mice treated with low protein diet

Project description:Nuclei of TAMs were sorted for single nucleus RNA sequencing from control-PyMT and MYC-PyMT tumor treated with low protein diet, and compare their transcriptome differences.

2023-04-24 | GSE230245 | GEO

The effect of imatinib therapy on tumor associated macrophages (TAMs) in murine gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs sorted from vehicle control tumors in GIST mice (Sommer et al, PNAS 2003) was compared to TAMs sorted from mice after 2 weeks of imatinib therapy The Affymetrix Mouse Genome 430A 2.0 platform was used Each treatment group had 8 mice. After 2 weeks of treatment, mice were sacrificed and tumors digested with collagenase. TAMs were then FACS sorted and pooled by group. Pooled groups were run in duplicate for the gene expression array.

2013-11-20 | E-GEOD-51698 | biostudies-arrayexpress

Expression data from in vitro-induced non-hypoxic tumour associated macrophages (TAMs)

Project description:Active immunotherapy is a promising strategy for anti-angiogenic cancer therapy. Recently, we have reported that a vaccine using human umbilical vein endothelial cells (HUVECs) induced specific anti-endothelial immune responses in the most of immunized patients, and resulted in tumor regression in some patients with recurrent malignant brain tumors, whereas not in colorectal cancer patients. In this study, we hypothesized that non-hypoxic perivascular tumor associated macrophages (TAMs) in colorectal cancer, but not in glioblastoma, might negatively alter the therapeutic efficacy of anti-angiogenic active immunotherapy. To test this hypothesis, we examined global gene expression profiles of non-hypoxic macrophages stimulated in vitro by soluble factors released from tumor cells of human glioblastoma U-87MG (‘brain TAMs’) or colorectal adenocarcinoma HT-29 (‘colon TAMs’). Murine non-hypoxic TAMs were induced in vitro by incubation with soluble factors released from human cancer cell lines U-87MG ('brain TAMs') or HT-29 ('colon TAMs'), for RNA extraction and subsequent hybridization on Affymetrix microarrays. To evaluate homogeneous macrophage populations at different tumour developmental stages, RNA aliquots of control macrophages and TAMs obtained at five different time-points, i.e. 8h, 16h, 24h, 32h and 40h, were pooled and used for screening of differentially expressed genes. The experiments for TAMs as well as for control unstimulated macrophages were performed in triplicates.

2012-03-31 | E-GEOD-18804 | biostudies-arrayexpress

Single cell sequencing of Tri-PyMT cells

Project description:To study the contribution of epithelial-to-mesenchymal transition (EMT) in tumor metastasis, we established an EMT lineage tracing model in a multiple-transgenic mouse (MMTV-PyMT/Fsp1-Cre/Rosa26mT/mG, Tri-PyMT). In this model, breast tumor cells that underwent EMT would irreversibly switch their expression of the fluorescent marker from RFP+ to GFP+ due to the mesenchymal specific Cre expression. Surprisingly, we found that metastatic tumor cells did not convert from RFP+ to GFP+. Lung metastases were predominantly composed of RFP+ tumor cells persistently exhibiting epithelial phenotypes. These findings challenge the concept that EMT is required for metastasis, and have attracted vigorous discussion about its true contributions to metastasis. One of the major concerns with the EMT lineage tracing model is that expression of GFP only indicates the complete EMT transition. The partial-EMT programming, a novel concept describing tumor cells exhibiting both epithelial and mesenchymal features, could possibly fail to launch the Fsp1-Cre-mediated fluorescent marker switch. To address this concern, we evaluated the EMT status of Tri-PyMT cells on the single cell level by performing single cell RNA-sequencing (scRNA-seq). We found that the expression of epithelial markers (i.e. Epcam and Krt18) and mesenchymal markers (i.e. Vim and S110a4) were largely confined to RFP+ and GFP+ subpopulations, respectively. Based on the differentially expressed EMT related genes, we observed an EMT spectrum in which the low EMT score end was enriched with RFP+ cells, whereas the high EMT score end was enriched with GFP+ cells. Indeed, the fluorescent marker switch in Tri-PyMT cells predicted their EMT status with high specificity and sensitivity. Tri-PyMT cells which were derived from the primary breast tumor of triple transgenic mouse (MMTV-PyMT:Fsp1-cre:Rosa26mT/mG) were sorted into RFP+ or GFP+ populations by FACS and subjected for Drop-seq analysis.

2022-02-01 | GSE126374 | GEO

Single cell RNA sequencing on PyMT mammary gland tumor cells

Project description:We labeled PyMT control cells versus PyMT-GPx2 KD with GFP in vitro and then injected into mammary fat pad of mice for incubating 45 days. We then generated single cell suspension by FACS sorting from PyMT-control, GPx2 KD. 10X Genomics was used to make cDNA library. We then sequenced the samples with Illumina high throughput sequencing.

2022-01-13 | GSE152368 | GEO

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