Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of pregnant and virgin mouse lung and liver

ABSTRACT: Metastasis depends on the ability of tumor cells to establish a relationship with the newly seeded host tissue that is conducive to their survival and proliferation. Recent evidence suggests that tumor cells regulate their own dissemination by preparing permissive “metastatic niches” within host tissues. However, the factors that are implicated in rendering tissues permissive for metastatic tumor growth have yet to be fully elucidated. Breast tumors arising during pregnancy display highly aggressive behaviour and early metastatic proclivity, raising the possibility that pregnancy may constitute a physiological condition of permissiveness for tumor dissemination. We show that during murine gestation, both the rate and degree of metastatic tumor growth are enhanced irrespective of tumor type and that decreased natural killer (NK) cell activity is responsible for the observed increase in experimental metastasis. We identify gene expression changes in pregnant mouse lung and liver that bear striking similarity with reported pre-metastatic niche signatures and several of the up-regulated genes are indicative of myeloid-cell infiltration. We provide evidence, that CD11b+ Gr-1+ myeloid-derived suppressor cells accumulate in pregnant mice and exert an inhibitory effect on NK cell activity, thereby enhancing metastatic tumor growth. MDSC have never been evoked in the context of pregnancy and our observations suggest that they may represent a further shared mechanism of immune suppression occurring during gestation and tumor growth.

ORGANISM(S): Mus musculus

PROVIDER: GSE18907 | GEO | 2011/03/19

SECONDARY ACCESSION(S): PRJNA121319

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of pregnant and virgin mouse lung and liver

Project description:Metastasis depends on the ability of tumor cells to establish a relationship with the newly seeded host tissue that is conducive to their survival and proliferation. Recent evidence suggests that tumor cells regulate their own dissemination by preparing permissive “metastatic niches” within host tissues. However, the factors that are implicated in rendering tissues permissive for metastatic tumor growth have yet to be fully elucidated. Breast tumors arising during pregnancy display highly aggressive behaviour and early metastatic proclivity, raising the possibility that pregnancy may constitute a physiological condition of permissiveness for tumor dissemination. We show that during murine gestation, both the rate and degree of metastatic tumor growth are enhanced irrespective of tumor type and that decreased natural killer (NK) cell activity is responsible for the observed increase in experimental metastasis. We identify gene expression changes in pregnant mouse lung and liver that bear striking similarity with reported pre-metastatic niche signatures and several of the up-regulated genes are indicative of myeloid-cell infiltration. We provide evidence, that CD11b+ Gr-1+ myeloid-derived suppressor cells accumulate in pregnant mice and exert an inhibitory effect on NK cell activity, thereby enhancing metastatic tumor growth. MDSC have never been evoked in the context of pregnancy and our observations suggest that they may represent a further shared mechanism of immune suppression occurring during gestation and tumor growth. Three chips were done per organ (liver/lung) and per condition (virgin/pregnant), with equal amounts of RNA from two mice pooled for one chip.

2011-03-19 | E-GEOD-18907 | biostudies-arrayexpress

Genomic profiling of human Tert/shp53/Ras mesenchymal cells isolated from several xenografted tumors and their non-transformant epithelial counterparts

Project description:The epithelial-mesenchymal transition (EMT) is an embryonic transdifferentiation program which consists of the conversion of polarized epithelial cells into a motile mesenchymal phenotype. EMT is aberrantly reactivated during tumor progression, promoting metastatic dissemination. Herein, we demonstrate that EMT-permissive conditions also favor tumor initiation by minimizing the number of events required for neoplastic transformation. We further demonstrated that even the partial commitment of human mammary epithelial cells into an EMT program is sufficient to confer malignant properties, suggesting that the reactivation of embryonic EMT inducers participates to the primary tumor growth long before the initiation of the invasion-metastasis cascade. arrayCGH profiles analysis of Tert/shp53/Ras epithelial HMEC derivatives and 3 different tumors generated after injection of mesenchymal Tert/shp53/Ras/ HMEC derivatives in fad pads of nude mice

2011-01-11 | E-GEOD-26534 | biostudies-arrayexpress

Gene expression profiles of p53 depleted human mammary epithelial cells with their Ras-infected epithelial and mesenchymal derivatives

2012-01-31 | GSE26541 | GEO

Genomic profiling of human Tert/shp53/Ras mesenchymal cells isolated from several xenografted tumors and their non-transformant epithelial counterparts

2011-01-11 | GSE26534 | GEO

Uterine transcriptome in b2m KO mice

Project description:Natural killer (NK) cell function is enhanced by interaction of inhibitory NK receptors with MHC class I molecules. NK cell function is critical during placentation, where these cells mediate adaptations to pregnancy in concert with other cells at the maternal/fetal interface. The aim of this experiment was to determine the downstream consequences on the uterine transcriptome that arise from lack of NK interaction with MHC class I molecules. This was done in mice lacking beta-2-microglobulin, thus not having correctly folded surface MHC class I. Biopsies were obtained from the mesometrial poles of the implantation chamber in gestation day (gd) 10.5 pregnant mice.

2018-11-01 | E-MTAB-4727 | biostudies-arrayexpress

Rhodes2019 - Immune-Mediated theory of Metastasis

Project description:Abstract: Accumulating experimental and clinical evidence suggest that the immune response to cancer is not exclusively anti-tumor. Indeed, the pro-tumor roles of the immune system - as suppliers of growth and pro-angiogenic factors or defenses against cytotoxic immune attacks, for example - have been long appreciated, but relatively few theoretical works have considered their effects. Inspired by the recently proposed "immune-mediated" theory of metastasis, we develop a mathematical model for tumor-immune interactions at two anatomically distant sites, which includes both anti- and pro-tumor immune effects, and the experimentally observed tumor-induced phenotypic plasticity of immune cells (tumor "education" of the immune cells). Upon confrontation of our model to experimental data, we use it to evaluate the implications of the immune-mediated theory of metastasis. We find that tumor education of immune cells may explain the relatively poor performance of immunotherapies, and that many metastatic phenomena, including metastatic blow-up, dormancy, and metastasis to sites of injury, can be explained by the immune-mediated theory of metastasis. Our results suggest that further work is warranted to fully elucidate the pro-tumor effects of the immune system in metastatic cancer.

2024-09-02 | BIOMD0000000926 | BioModels

Stromal Changes in The Aged Lung Induce an Emergence From Melanoma Dormancy

Project description:Disseminated cancer cells (DCCs) that escape the primary site can seed in distal tissues, but may take several years, or even decades to grow out into overt metastases, a phenomenon termed tumor dormancy. Despite its importance in metastasis and residual disease, few studies have been able to successfully model or characterize dormancy within melanoma. Here, we show that age-related changes in the lung microenvironment facilitate a permissive niche for efficient outgrowth of disseminated dormant tumor cells, in contrast to the aged skin, where age-related changes suppress melanoma growth but drive dissemination. A model of melanoma progression that addresses these microenvironmental complexities is the phenotype switching model, which argues that melanoma cells switch between a proliferative cell state and a slower-cycling, invasive state1-3. We have previously shown that dermal fibroblasts are key orchestrators of promoting phenotype switching in primary melanoma tumors via changes in the secretion of soluble factors during aging4-8. Our new data identifies Wnt5A as a master regulator of activating melanoma DCC dormancy within the lung, which initially enables efficient dissemination and seeding of melanoma cells in metastatic niches. Age-induced reprogramming of lung fibroblasts increases their secretion of the soluble Wnt antagonist sFRP1, which inhibits Wnt5A, enabling efficient metastatic outgrowth. Further, we have identified the tyrosine kinase receptors AXL and MER as promoting a dormancy-toreactivation axis respectively. Overall, we find that age-induced changes in distal metastatic microenvironments promotes efficient reactivation of dormant melanoma cells in the lung.

2022-03-03 | MSV000088977 | MassIVE

Gene expression profiles of p53 depleted human mammary epithelial cells with their Ras-infected epithelial and mesenchymal derivatives

Project description:The epithelial-mesenchymal transition (EMT) is an embryonic transdiffrentiation program which consists of the conversion of polarized epithelial cells into a motile mesenchymal phenotype. EMT is aberrantly reactivated during tumor progression, promoting metastatic dissemination. Herein, we demonstrate that EMT permissive conditions also favor tumor initiation by minimizing the number of events required for neoplastic transformation. We further demonstrated that even partial commitment of human mammary epithelial cells into an EMT program is sufficient to confer malignant properties, suggesting that the reactivation of embryonic EMT inducers participate to the primary tumor growth long before the initiation of the invasion-metastasis cascade. Human mammary epithelial cells (HMEC) were sequentially depleted in p53 through RNA interference (shp53), transduced with H-RasG12V and immortalized by hTert. Two different Tert/shp53/Ras cell population emerge that display either an epithelial (Epi) or a mesenchymal (Mes) phenotype. Gene expression profiles of the Tert/shp53 control cells and of tert/shp53/Ras/Epi and Tert/shp53/Ras/Mes were analyzed.

2012-01-31 | E-GEOD-26541 | biostudies-arrayexpress

Proteomics of early pregnancy maternal serum from preeclampsia and normal pregnancies

Project description:We performed a LC-FAIMS-MS proteomics of early pregnancy (11–14 weeks of gestation) serum from the pregnant women who developed preeclampsia (n = 11) and those from the noraml pregnant women (n = 12).

2022-12-16 | PXD038873 |

The platelet releasate (PR) in human pregnancy

Project description:Healthy pregnancy is characterized by an increase in platelet activation and a decrease in the number of circulating platelets with gestation. Despite this recognised importance, proteomic studies investigating platelets in healthy pregnancy have not been performed. As platelet cargo can be altered in different conditions, we hypothesised that platelets may store a relevant and bespoke collection of molecules during pregnancy. To examine this, we performed comparative label-free quantitative proteomic profiling of platelet releasates from healthy pregnant and non-pregnant women using a tandem mass spectrometry approach. Of the 723 proteins identified, 69 PR proteins were found to be differentially released from platelets in pregnancy, including proteins only expressed during pregnancy such as pregnancy-specific glycoproteins and human placental lactogen.

2020-06-05 | PXD009361 | Pride

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