Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modulating Immune Cells to Prevent Breast Cancer Lung Metastasis

ABSTRACT: Modulating Immune Cells to Prevent Breast Cancer Lung Metastasis

PROVIDER: PRJNA436027 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6784720.fastq.gz	Fastqsanger.gz
	SRR6784721.fastq.gz	Fastqsanger.gz
	SRR6784722.fastq.gz	Fastqsanger.gz
	SRR6784723.fastq.gz	Fastqsanger.gz
	SRR6784724.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

Modulating Immune Cells to Prevent Breast Cancer Lung Metastasis

Project description:Current lack of insight into mechanisms governing breast cancer metastasis has precluded development of curative therapies. Metastasis-initiating cells (MICs) are cancer cells uniquely equipped to establish metastatic outgrowths and are thought to cause recurrence and therapeutic resistance. Using various models of early metastatic disease, we have uncovered mechanisms by which certain primary tumors can prevent MICs from generating secondary tumors. In such cases, the primary tumor elicits a systemic immune response involving IL-1β expressing innate inflammatory cells that infiltrate the distant MIC microenvironment. Elevated IL-1β levels at the metastatic site prevent MICs from generating their highly proliferative E-cadherin-positive epithelial progeny. Thus, when the inherent plasticity of MICs is impeded, robustly growing tumors cannot be established. Ablation of the pro-inflammatory response or IL-1R inhibition relieves the block in differentiation and results in MIC colonization. Our data reveal complex and potentially life-prolonging interactions that occur between primary tumors and disseminated MICs that could be exploited to improve survival of patients at risk for metastatic disease.

2018-06-26 | GSE111157 | GEO

Modulating Bone Marrow Hematopoietic Lineage Potential to Prevent Breast Cancer Bone Metastasis

Project description:Modulating Bone Marrow Hematopoietic Lineage Potential to Prevent Breast Cancer Bone Metastasis

| PRJNA422921 | ENA

Lung metastasis of breast cancer

Project description:Lung metastasis of breast cancer

| PRJNA499112 | ENA

SCUBE2 mediates bone metastasis of luminal breast cancer by modulating immune-suppressive osteoblastic niches

Project description:SCUBE2 mediates bone metastasis of luminal breast cancer by modulating immune-suppressive osteoblastic niches

| PRJNA773046 | ENA

SCUBE2 mediates bone metastasis of luminal breast cancer by modulating immune-suppressive osteoblastic niches

Project description:Estrogen receptor (ER)-positive luminal breast cancer is a subtype with generally lower risk of metastasis to most distant organs. However, bone recurrence occurs preferentially in luminal cancer. The mechanisms of the subtype-specific organotropism remain elusive. Here we show that an ER-regulated secretory protein SCUBE2 contributes to bone tropism of luminal breast cancer. Single-cell RNA sequencing analysis reveals osteoblastic enrichment by SCUBE2 in early bone-metastatic niches. SCUBE2 facilitates release of tumor membrane-anchored SHH to activate Hedgehog signaling in mesenchymal stem cells, thus promoting osteoblast differentiation. Osteoblasts deposit collagens to suppress NK cells via the inhibitory LAIR1 signaling and promote tumor colonization. SCUBE2 expression and secretion are associated with osteoblast differentiation and bone metastasis in human tumors. Targeting Hedgehog by Sonidegib and targeting SCUBE2 with a neutralizing antibody both effectively suppress bone metastasis in multiple metastasis models. Overall, our findings provides an explanation for bone preference in luminal breast cancer and new approaches for metastasis treatment.

2023-04-15 | GSE186230 | GEO

Modulating Bone Marrow Hematopoietic Lineage Potential to Prevent Breast Cancer Bone Metastasis

Project description:The presence of disseminated tumor cells in patient bone marrow (BM) aspirates predicts decreased recurrence-free survival, yet little is known about whether hematopoietic BM cells impact bone metastases. Here, we report that the BM can be rendered metastasis-suppressive by the bone-targeting bisphosphonate, zoledronic acid (ZA). In particular, ZA modulates hematopoietic myeloid/osteoclast progenitor cell (M/OCP) lineage potential to render them metastasis-suppressive. Granulocyte-colony stimulating factor (G-CSF) promotes resistance to ZA by re-directing M/OCP differentiation. We identified BM transcriptional programs that associate with metastasis suppression and resistance to ZA. Analysis of patient blood samples taken at randomization revealed that women with plasma G-CSF levels >23 pg/mL experienced significantly worse outcome with adjuvant ZA than those on ZA who had lower plasma G-CSF levels. Our findings establish that hematopoietic cells and M/OCP lineage potential profoundly impact bone metastasis and support the discovery of biomarkers that stratify therapeutic responses in patients at risk of recurrence.

2021-02-25 | GSE108250 | GEO

Breast cancer brain metastasis

Project description:Breast cancer brain metastasis

| PRJNA970206 | ENA

Non-immune niche analysis in breast tumour derived lung metastasis

Project description:Non-immune niche analysis in breast tumour derived lung metastasis

| PRJNA543884 | ENA

RECK Controls Breast Cancer Metastasis by Modulating a Convergent, STAT3-dependent Neoangiogenic Switch

Project description:Metastasis leads to the majority of deaths in breast cancer patients. Here we investigated the molecular and biochemical signaling pathways altered by RECK, a major metastasis suppressor gene in breast cancer. We overexpressed RECK in 2 highly invasive cell lines and knocked-down RECK expression in 2 poorly invasive cell lines. IPA analysis of differentially expressed genes revealed IL-6, and IL8 signaling alteration with RECK pertubation. This lead us to discover that RECK suppresses metastasis and neoangiogenesis at secondary sites by inhibiting STAT3 dependent VEGF & uPA regulating. This finding is significant because it reveals the biology behind a major metastasis suppressor gene in cancer. Cell lines were obtained from the ATCC or were generous gifts from Dr Joan Massague (MSKCC). Invasive cell lines were stably infected with a constitutively expressing RECK construct or and Empty Vector control. Poorly invasive cell lines were transfected with a Scramble siRNA or siRNA targeting the RECK gene. RNA was extracted using the RNeasy kit (Qiagen) as per the manufacturer’s instructions. Expression analysis was performed using the Affymetrics U133 2.0 microarray (Affymetrix). Affymetrix CEL files were imported into the Partek Genomics Suite (Partek).

2014-09-01 | E-GEOD-56898 | biostudies-arrayexpress

Snord67 promotes breast cancer metastasis by guiding U6 modification and modulating the splicing landscape

Project description:Snord67 promotes breast cancer metastasis by guiding U6 modification and modulating the splicing landscape

| PRJNA1147254 | ENA