Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Murine ML-DS-like leukemias

ABSTRACT: Modelling the progression from TAM to ML-DS in children with Down syndrome utilizing a murine transplantation model

PROVIDER: PRJEB30376 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3001940.fastq.gz	Fastqsanger.gz
	ERR3001950.fastq.gz	Fastqsanger.gz
	ERR3001960.fastq.gz	Fastqsanger.gz
	ERR3001970_1.fastq.gz	Fastqsanger.gz
	ERR3001970_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 74

Similar Datasets

RNA sequencing data from Myeloid Leukaemia of Down Syndrome (ML-DS)

Project description:RNA sequencing data from Myeloid Leukaemia of Down Syndrome (ML-DS)

| PRJEB32403 | ENA

Transcriptome analysis of cell line/patient-derived xenograft (PDX) samples of myeloid leukemia associated with Down syndrome (ML-DS)

Project description:Myeloid leukemia associated with Down syndrome (ML-DS) is a rare pediatric cancer in which 10-20% patients who are relapsed/refractory have very limited treatment options. Novel treatment options may be identified via transcriptome profiling.

2026-06-18 | GSE271179 | GEO

Multiplexed DNA high throughput genotyping study to determine the mutational status of transient (TAM) and acute myeloid leukaemic (ML-DS) Down syndrome individuals.

Project description:We used a 48.48 Fluidigm Access Array approach (1070 Amplicons spanning 62 genes: 157kB coverage) of genomic DNA from over 100 samples to genotype individuals with transient abnormal myelopoiesis (TAM) and acute myeloid leukemia of Down syndrome (ML-DS). Individually barcoded patient samples were subjected to paired-end 150bp sequencing (Illumina MiSeq), including paired GATA1 variant negative controls (including Post treatment) and 8 known reference GATA1- controls. Samples were mapped to build 37 of the human reference genome and subject to bioinformatic analysis (Varscan, Pindel, GATK) to facilitate the characterisation of known gene mutations in cancer as well as the identification / validation of potentially novel variants.

2019-07-17 | E-MTAB-7729 | biostudies-arrayexpress

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome [Hi-C]

Project description:Children with Down syndrome have a 150-fold increased risk of developing the myeloid leukemia of Down syndrome (ML-DS). ML-DS is preceded by transient abnormal myelopoiesis (TAM), which spontaneously resolves in most cases but progresses to AML with additional mutations most commonly in the cohesin complex or signaling genes. However, the mechanisms by which these alterations promote leukemia are unknown. Here, we leveraged isogenic cell lines and patient data to investigate the role of cohesin mutations in leukemia progression. Multi-omic analyses revealed that haploinsufficiency of the cohesin complex suppresses the occupancy of CIITA at HLA class II loci, leading to a reduction in HLA Class II gene expression. Surface levels of HLA-DR are lower in ML-DS relative to TAM and these decreased levels are associated with an increased risk of TAM progression. Of note, a decrease in HLA-Class II gene expression is also a feature of non-DS AML with reduced expression of cohesin family members. These data suggest that unlike TAM, ML-DS blasts may evade the immune system by reduced HLA class II expression, providing a new model for leukemia progression in DS.

2026-07-20 | GSE314940 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome [ChIP-seq]

2026-07-20 | GSE314929 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome. [CRISPR]

2026-07-20 | GSE314927 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome. [ATAC-Seq]

2026-07-20 | GSE314926 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome [CUT&Run]

2026-07-20 | GSE314930 | GEO

Cohesin mutations suppress HLA class II gene expression to promote immune evasion during the progression to acute leukemia in children with Down syndrome. [RNA-Seq]

2026-07-20 | GSE314928 | GEO

Affymetrix SNP array data for xenografted transient abnormal myelopoiesis samples

Project description:Transient abnormal myelopoiesis (TAM) is a clonal pre-leukemic disorder that progresses to myeloid leukemia of Down syndrome (ML-DS) through the accumulation of genetic alterations. To investigate the mechanism of leukemogenesis in this disorder, a xenograft model of TAM was established using NOD/Shi-scid, IL-2Rγnull mice. In serial transplantations, engrafted TAM-derived cells showed the emergence of divergent subclones with another GATA1 mutation and various CNAs, including a 16q deletion and 1q gain, which are clinically associated with ML-DS. These results suggest that genetically heterogeneous subclones with varying leukemia-initiating potential already exist in the neonatal TAM phase, and ML-DS may develop from a pool of such minor clones through clonal selection.

2013-03-01 | GSE44739 | 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