Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

In-Vivo Expansion of Cancer Stemness Affords Novel Cancer Stem Cell Targets: Malignant Rhabdoid Tumor as an Example

ABSTRACT: In-Vivo Expansion of Cancer Stemness Affords Novel Cancer Stem Cell Targets: Malignant Rhabdoid Tumor as an Example

PROVIDER: PRJNA471507 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7166070.fastq.gz	Fastqsanger.gz
	SRR7166080.fastq.gz	Fastqsanger.gz
	SRR7166071.fastq.gz	Fastqsanger.gz
	SRR7166081.fastq.gz	Fastqsanger.gz
	SRR7166072.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

In-Vivo Expansion of Cancer Stemness Affords Novel Cancer Stem Cell Targets: Malignant Rhabdoid Tumor as an Example

Project description:Cancer stem cell (CSC) identification relies on transplantation assays of cell sub-populations sorted from fresh tumor samples. Herein, we attempt to bypass limitations of abundant tumor source and predetermined immune selection by in-vivo propagating patient derived xenografts (PDX) from human malignant rhabdoid tumor (MRT), a rare and lethal pediatric neoplasm, to an advanced state in which most cells behave as CSCs. Stemness is then probed by comparative transcriptomics of serial PDXs generating a gene signature of EMT, invasion/motility, metastasis and self-renewal, pinpointing putative MRT CSC markers. The relevance of these putative CSC molecules is analyzed by sorting tumorigenic fractions from early-passaged PDX according to one such molecule, deciphering expression in archived primary tumors and testing the effects of CSC molecule inhibition on MRT growth. Using this platform, we identify ALDH1 and lysyl oxidase (LOX) as relevant targets and provide a larger framework for target and drug discovery in rare pediatric cancers.

2018-06-01 | GSE114471 | GEO

In Vivo Expansion of Cancer Stemness Affords Novel Cancer Stem Cell Targets: Malignant Rhabdoid Tumor as an Example.

Project description:Cancer stem cell (CSC) identification relies on transplantation assays of cell subpopulations sorted from fresh tumor samples. Here, we attempt to bypass limitations of abundant tumor source and predetermined immune selection by in vivo propagating patient-derived xenografts (PDX) from human malignant rhabdoid tumor (MRT), a rare and lethal pediatric neoplasm, to an advanced state in which most cells behave as CSCs. Stemness is then probed by comparative transcriptomics of serial PDXs generating a gene signature of epithelial to mesenchymal transition, invasion/motility, metastasis, and self-renewal, pinpointing putative MRT CSC markers. The relevance of these putative CSC molecules is analyzed by sorting tumorigenic fractions from early-passaged PDX according to one such molecule, deciphering expression in archived primary tumors, and testing the effects of CSC molecule inhibition on MRT growth. Using this platform, we identify ALDH1 and lysyl oxidase (LOX) as relevant targets and provide a larger framework for target and drug discovery in rare pediatric cancers.

| S-EPMC6135722 | biostudies-literature

Methylation profiling of Malignant Rhabdoid Tumours

Project description:An observational experiment to methylation profile 79 SMARCB1 negative primary tumours from patients diagnosed with Malignant Rhabdoid Tumours.

2020-07-15 | E-MTAB-6708 | biostudies-arrayexpress

RNA-seq profiling of Malignant Rhabdoid Tumours

Project description:An observational experiment to methylation profile 23 SMARCB1 negative primary tumours from patients diagnosed with Malignant Rhabdoid Tumours.

2024-12-31 | E-MTAB-6775 | biostudies-arrayexpress

Soil example

Project description:Soil example Raw sequence reads

| PRJNA710800 | ENA

Soil example

Project description:Soil example Raw sequence reads

| PRJNA678825 | ENA

Soil example

Project description:Soil example Raw sequence reads

| PRJNA711456 | ENA

Global Chromatin Changes resulting from Single Gene Inactivation – the Role of SMARCB1 in Malignant Rhabdoid Tumor

Project description:Human cancer typically results from the stochastic accumulation of multiple oncogene-activating and tumors suppressor gene inactivating mutations, however this process takes time and especially in the context of certain pediatric cancer, fewer but more ‘impactful’ mutations may in short order produce the full-blown cancer phenotype. This is well-exemplified by the highly aggressive malignant rhabdoid tumor (MRT), where the only gene classically showing recurrent inactivation is SMARCB1, a subunit member of the BAF chromatin remodeling complex. This is true of all three presentations of MRT including MRT of kidney (MRTK), MRT of the central nervous system (Atypical Teratoid Rhabdoid Tumor – ATRT) and Extracranial, Extrarenal Rhabdoid Tumor (EERT). Our reverse modeling of rhabdoid tumors with isogenic cell lines, either induced or not induced, to express SMARCB1 showed widespread differential chromatin remodeling indicative of altered BAF complex activity with ensuant histone modifications when tested by chromatin immunoprecipitation followed by sequencing (ChIP-seq). The changes due to reintroduction of SMARCB1 were preponderantly at typical enhancers with tandem BAF complex occupancy at these sites and related gene activation, as substantiated also by transcriptomic data. Indeed, for both MRTK and ATRT cells, there is evidence of an overlap between SMARCB1-dependent enhancer activation and tissue-specific lineage determining genes. These genes are inactive in the tumor state, conceivably arresting the cells in a primitive/undifferentiated state. This epigenetic dysregulation from inactivation of a chromatin remodeling complex subunit contributes to an improved understanding of the complex pathophysiological basis of MRT, one of the most lethal and aggressive human cancers.

2021-05-15 | GSE174446 | GEO

DNA methylation profiling of SMARCB1 reconstitution in malignant rhabdoid tumor organoids

Project description:We have generated DNA methylation profiles for patient-derived malignant rhabdoid tumor organoids and re-expressed SMARCB1 to assess SMARCB1-dependent changes in DNA methylation

2021-01-13 | GSE161814 | GEO

FIBP maintains colorectal cancer cells stemness via demethylation of stemness genes

Project description:FIBP maintains colorectal cancer cells stemness via demethylation of stemness genes

| PRJNA412214 | ENA