Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE115356 | GEO | 2018/11/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

T-ALL leukemia stem cell 'stemness' is epigenetically controlled by the master regulator SPI1.

Project description:Leukemia stem cells (LSCs) are regarded as the origins and key therapeutic targets of leukemia, but limited knowledge is available on the key determinants of LSC 'stemness'. Using single-cell RNA-seq analysis, we identify a master regulator, SPI1, the LSC-specific expression of which determines the molecular signature and activity of LSCs in the murine Pten-null T-ALL model. Although initiated by PTEN-controlled β-catenin activation, Spi1 expression and LSC 'stemness' are maintained by a β-catenin-SPI1-HAVCR2 regulatory circuit independent of the leukemogenic driver mutation. Perturbing any component of this circuit either genetically or pharmacologically can prevent LSC formation or eliminate existing LSCs. LSCs lose their 'stemness' when Spi1 expression is silenced by DNA methylation, but Spi1 expression can be reactivated by 5-AZ treatment. Importantly, similar regulatory mechanisms may be also present in human T-ALL.

| S-EPMC6251627 | biostudies-literature

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [bulkRNA]

Project description:Leukemia stem cells (LSCs) are regarded as the origins and key therapeutic targets of leukemia, but limited knowledge is available on the key determinants of LSC “stemness”. Using single cell RNAseq analysis, we identify a master regulator PU.1, whose LSC-specific expression determines the molecular signature and activity of LSC in the Pten-null T-ALL model. Although initiated by PTEN controlled β-catenin activation, PU.1 expression and LSC “stemness” are maintained by a β-catenin-PU.1-TIM-3 feedback loop, independent of the leukemogenic driver mutation. Perturbing any component of this loop, either genetically or pharmacologically, can prevent LSC formation or eradicate existing LSCs. LSCs lose their “stemness” when PU.1 expression is silenced by DNA methylation, which can be reactivated by 5-AZ. Importantly similar regulatory mechanisms are also present in human T-ALLs.

2018-11-17 | GSE115346 | GEO

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [BiSulfite-seq]

Project description:Leukemia stem cells (LSCs) are regarded as the origins and key therapeutic targets of leukemia, but limited knowledge is available on the key determinants of LSC “stemness”. Using single cell RNAseq analysis, we identify a master regulator PU.1, whose LSC-specific expression determines the molecular signature and activity of LSC in the Pten-null T-ALL model. Although initiated by PTEN controlled β-catenin activation, PU.1 expression and LSC “stemness” are maintained by a β-catenin-PU.1-TIM-3 feedback loop, independent of the leukemogenic driver mutation. Perturbing any component of this loop, either genetically or pharmacologically, can prevent LSC formation or eradicate existing LSCs. LSCs lose their “stemness” when PU.1 expression is silenced by DNA methylation, which can be reactivated by 5-AZ. Importantly similar regulatory mechanisms are also present in human T-ALLs.

2018-11-17 | GSE115316 | GEO

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [scRNA-seq]

Project description:Leukemia stem cells (LSCs) are regarded as the origins and key therapeutic targets of leukemia, but limited knowledge is available on the key determinants of LSC “stemness”. Using single cell RNAseq analysis, we identify a master regulator PU.1, whose LSC-specific expression determines the molecular signature and activity of LSC in the Pten-null T-ALL model. Although initiated by PTEN controlled β-catenin activation, PU.1 expression and LSC “stemness” are maintained by a β-catenin-PU.1-TIM-3 feedback loop, independent of the leukemogenic driver mutation. Perturbing any component of this loop, either genetically or pharmacologically, can prevent LSC formation or eradicate existing LSCs. LSCs lose their “stemness” when PU.1 expression is silenced by DNA methylation, which can be reactivated by 5-AZ. Importantly similar regulatory mechanisms are also present in human T-ALLs.

2018-11-17 | GSE115350 | GEO

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1

Project description:T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1

| PRJNA474680 | ENA

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [bulkRNA]

Project description:T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [bulkRNA]

| PRJNA474666 | ENA

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [scRNA-seq]

Project description:T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [scRNA-seq]

| PRJNA474678 | ENA

T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [BiSulfite-seq]

Project description:T-ALL Leukemia Stem Cell “stemness” is Epigenetically Controlled by the Master Regulator PU.1 [BiSulfite-seq]

| PRJNA474659 | ENA

Pruning of the adipocyte cistrome by hematopoietic master regulator PU.1

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-27 | E-GEOD-48345 | biostudies-arrayexpress

Pruning of the adipocyte cistrome by hematopoietic master regulator PU.1

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-06-27 | GSE48345 | 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