Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phenotypic states of leptomeningeal metastasis

ABSTRACT: Phenotypic states of leptomeningeal metastasis

PROVIDER: PRJNA564289 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10079366_1.fastq.gz	Fastqsanger.gz
	SRR10079366_2.fastq.gz	Fastqsanger.gz
	SRR10079367_1.fastq.gz	Fastqsanger.gz
	SRR10079367_2.fastq.gz	Fastqsanger.gz
	SRR10079368_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Phenotypic states of leptomeningeal metastasis

Project description:Leptomeningeal metastasis (LM), or spread of cancer cells into the cerebrospinal fluid, is characterized by a rapid onset of debilitating neurological symptoms and markedly bleak prognosis. The lack of reproducible in vitro and in vivo models has prevented development of novel, LM-specific therapies. Although LM allows for longitudinal sampling of floating cancer cells with a spinal tap, attempts to culture patient-derived leptomeningeal cancer cells have not been successful. We therefore employ leptomeningeal derivatives of human breast and lung cancer cell lines that reproduce both floating and adherent phenotypes of human LM in vivo and in vitro. We introduce a trypsin/EDTA-based fractionation method to reliably separate the two cell subsets and demonstrate that in vitro cultured floating cells have decreased proliferation rate, lower ATP content, and are enriched in distinct metabolic signatures. Long-term fractionation and transcriptomic analysis suggest a high degree plasticity between the two phenotypes in vitro. Floating cells colonize mouse leptomeninges more rapidly and associate with shortened survival. In addition, patients harboring LM diagnosed with CSF disease alone succumbed to the disease earlier than patients with adherent (MRI-positive) disease. Together, these data support mechanistic evidence of a metabolic adaptation that allows cancer cells to thrive in their natural environment but leads to death in vitro.

2020-01-21 | GSE137020 | GEO

Cerebrospinal fluid microRNA profile in leptomeningeal metastasis patients [LM vs non-LM]

Project description:This study aimed to identify specific CSF miRNAs for diagnosing and monitoring leptomeningeal metastasis with lung adenocarcinoma. In discovery phase, we performed miRNA microarray analysis in CSF samples from leptomeningeal metastasis patients and non-leptomeningeal metastasis controls.

2020-02-26 | GSE125191 | GEO

Cerebrospinal fluid microRNA profile in leptomeningeal metastasis patients [pre- vs post-treatment]

Project description:This study aimed to identify specific CSF miRNAs for diagnosing and monitoring leptomeningeal metastasis with lung adenocarcinoma. In discovery phase, we performed miRNA microarray analysis in matched CSF samples from leptomeningeal metastasis patients at diagnosis and after initial leptomeningeal metastasis-directed therapy.

2020-02-26 | GSE125192 | GEO

Single-cell atlas of human leptomeningeal metastasis

Project description:Single-cell atlas of human leptomeningeal metastasis

| PRJNA633130 | ENA

RNA profiling of CSF resident macrophages and monocyte-macrophages from leptomeningeal metastasis mice

Project description:We investigated the functional effect of dura-derived leptomeningeal matastasis (LM)-associated macrophages (dLAMs) on the cerebrospinal fluid (CSF) niche during LM outgrowth. Using lung cancer leptomeningeal metastasis models of Cx3cr1CreER:mTmG mice with tamoxifen administration, we achieved dLAMs and monocyte-macrophages via fluorescence-activated cell sorting (FACS). Then we performed bulk RNAseq analysis for these two cell populations.

2024-07-24 | GSE267325 | GEO

Single-cell atlas of dura cells from non-tumor or leptomeningeal metastasis mice

Project description:We performed scRNA-seq on the cells isolated from the dura mater in non-tumor control mice and leptomeningeal metastasis (LM) mice with LLC-LeptoM cell inoculation for 7 or 12 days.

2024-07-24 | GSE267322 | GEO

Immunocompetent models of brain parenchymal and leptomeningeal metastasis

Project description:Immunocompetent models of brain parenchymal and leptomeningeal metastasis

| PRJNA913954 | ENA

Cerebrospinal fluid microRNA profile in leptomeningeal metastasis patients

Project description:Cerebrospinal fluid microRNA profile in leptomeningeal metastasis patients

| PRJNA515498 | ENA

Genes that mediate leptomeningeal metastasis from breast and lung solid tumor primaries

Project description:Little is understood about the gene expression changes that underlie cancer spread to the cerebrospinal fluid, or leptomeningeal metastasis. Using four cancer cell line models, we empolyed iterative in vivo selection to generate subpopulations of these cell lines able to access the leptomeningeal space and grow once there. We compared the gene expression profile of the terminally selected cells or "Lep" cells with that of the parental or "Par" cells, as well as that of an intermediate stage of in vivo selection or "Int" cells. Analyses for brain parenchymal metastatic derivatives or "BrM" cells were included for comparison.

2017-05-10 | GSE83132 | GEO

Single-cell atlas of human leptomeningeal metastasis

Project description:The tumor microenvironment plays a critical regulatory role in cancer progression, especially in metastases to the central nervous system. Cancer cells inhabiting the cerebrospinal spinal fluid (CSF)-filled leptomeningeal space face substantial microenvironmental challenges including inflammation and sparse extracellular iron. Unlike CSF leukocytes, we find that cancer cells within the CSF express the iron-binding protein LCN2 and its receptor SCL22A17. Employing mouse models of LM, we find that the LCN2/SLC22A17 system is necessary to support leptomeningeal cancer cell growth. We find that infiltrating CSF macrophages generate inflammatory cytokines that induce cancer cell LCN2 expression. This LCN2/SLC22A17 system provides cancer cells superior access to limiting extracellular iron, allowing LCN2-expressing cancer cells to outcompete CSF macrophages for this resource. Finally, pharmacologic interruption of these interactions prevents cancer cell growth within the leptomeninges.

2020-07-16 | GSE150660 | 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