Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: PRC2 Inhibitors Overcome Glucocorticoid Resistance Driven by NSD2 Mutation in Pediatric Acute Lymphoblastic Leukemia

PROVIDER: PRJNA669144 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12833200_1.fastq.gz	Fastqsanger.gz
	SRR12833200_2.fastq.gz	Fastqsanger.gz
	SRR12835000_1.fastq.gz	Fastqsanger.gz
	SRR12835000_2.fastq.gz	Fastqsanger.gz
	SRR12851600_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 240

Similar Datasets

Defining the NSD2 interactome: PARP1 PARylation reduces NSD2 histone methyltransferase activity and impedes chromatin binding

Project description:NSD2 is a histone methyltransferase that specifically dimethylates histone H3 lysine 36 (H3K36me2), a modification associated with gene activation. Dramatic overexpression of NSD2 in t(4;14) multiple myeloma (MM) and an activating mutation of NSD2 discovered in acute lymphoblastic leukemia (ALL) are significantly associated with altered gene activation, transcription and DNA damage repair. The partner proteins through which NSD2 may influence critical cellular processes remain poorly defined. In this study, we utilized proximity-based labelling (BioID) combined with label-free quantitative mass spectrometry to identify high confidence NSD2 interacting partners in MM cells.

2019-06-27 | PXD013759 | Pride

Whole-genome GR binding sites and histone acetylation status in pediatric acute lymphoblastic leukemia patient-derived xenografts following dexamethasone treatment in vivo

2014-12-18 | GSE58266 | GEO

Persistence of targetable lesions, predicted therapy sensitivity and proteomes through disease evolution in pediatric acute lymphoblastic leukemia

Project description:This data set consists of pediatric acute lymphoblastic leukemia (ALL) primary bone marrow biopsies from the BC Children's Hospital BioBank, pediatric ALL cell lines, non-cancer bone marrow biopsies, and few ALL PDX. All files are DIA and searched by Spectronaut with a spectral library.

2023-01-05 | MSV000091012 | MassIVE

Whole-genome GR binding sites and histone acetylation status in pediatric acute lymphoblastic leukemia patient-derived xenografts following dexamethasone treatment in vivo

Project description:Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). However, the signaling pathways regulating apoptosis in glucocorticoid-treated lymphoid cells remain unclear. In this study, pediatric ALL patient-derived xenograft inherently sensitive to glucocorticoids were exposed to dexamethasone in vivo. Whole-genome GR binding sites and histone acetylation status were detected using chromatin immunoprecipitation sequencing analyses. This provided a global understanding of dexamethasone-induced DNA modulations in ALL cells in vivo, which is likely to be important in the understanding of mechanisms of glucocorticoid response in lymphoid malignancies. One xenograft (ALL-54) was derived from a patient of dexamethasone-good responder. The xenograft was innoculated into 2 NOD/SCID mice, and treated with dexamethasone (15 mg/kg) or vehicle control. Binding of glucocorticoid receptor (GR), histone acetylation and IgG control in spleen-harvest xenograft samples were detected using ChIP-seq.

2014-12-18 | E-GEOD-58266 | biostudies-arrayexpress

Expression of DND41 cell lines treated with 1M-BM-5M Dexamethasone for 24h after shPTEN infection

Project description:Glucocorticoid resistance is a major driver of therapeutic failure in T-cell acute lymphoblastic leukemia (T-ALL). Here we identify the AKT1 kinase as a signaling factor driving glucocorticoid resistance in T-ALL. Mechanistically, AKT1 directly phosphorylates the glucocorticoid receptor NR3C1 protein and blocks glucocorticoid-induced NR3C1 transcription by inhibiting glucocorticoid-induced NT3C1 translocation to the nucleus. Consistently, pharmacologic inhibition of AKT1 increases the response of T-ALL cells to glucocorticoid therapy and effectively reverses glucocorticoid resistance in vitro and in vivo. These results warrant the clinical testing of AKT1 inhibitors and glucocorticoids in combination for the treatment of T-ALL. Gene Expression Analysis of DND41 cell lines infected with shPTEN or shLUC and treated with 1M-BM-5M Dexamethasone vs DMSO for 24h, in triplicate.

2013-10-01 | E-GEOD-41062 | biostudies-arrayexpress

Integrated Genomic Analysis of Relapsed Childhood Acute Lymphoblastic Leukemia reveals therapeutic strategies

Project description:This SuperSeries is composed of the following subset Series: GSE28460: Expression data from ALL diagnosis and relapse pediatric acute lymphoblastic leukemia cases GSE28461: Promoter methylation data from ALL diagnosis and relapse pediatric acute lymphoblastic leukemia cases Refer to individual Series

2011-09-22 | E-GEOD-28462 | biostudies-arrayexpress

Expression of DND41 cell lines treated with 1µM Dexamethasone for 24h after shPTEN infection

2013-10-01 | GSE41062 | GEO

MicroRNA-sequencing of Brazilian pediatric acute lymphoblastic leukemia

Project description:MicroRNA-sequencing of the bone marrow samples from Brazilian pediatric patients with B-cell acute lymphoblastic leukemia (B-ALL) and T-cell acute lymphoblastic leukemia (T-ALL).

2022-04-13 | E-MTAB-11621 | biostudies-arrayexpress

in vivo dexamethasone-induced gene expression in pediatric acute lymphoblastic leukemia patient-derived xenografts

Project description:Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). The pro-apoptotic BIM protein is an important mediator of glucocorticoid-induced apoptosis in normal and malignant lymphocytes, while the anti-apoptotic BCL2 confers resistance. The signaling pathways regulating BIM and BCL2 expression in glucocorticoid-treated lymphoid cells remain unclear. In this study, pediatric ALL patient-derived xenografts (PDXs) inherently sensitive or resistant to glucocorticoids were exposed to dexamethasone in vivo. In order to understand the basis for differential in vivo glucocorticoid sensitivity of PDXs, microarray analysis of gene expression was carried out on 5 each of dexamethasone-sensitive and resistant PDXs . This provided a global understanding of dexamethasone-induced signaling cascades in ALL cells in vivo, and especialy identified the genes that are involved in transducing the apoptotic signal, upstream of BIM/BCL2 dynamic interactions.

2014-05-20 | GSE57795 | GEO

NSD2 E1099K drives relapse in pediatric acute lymphoblastic leukemia by disrupting 3D chromatin organization

Project description:NSD2 E1099K drives relapse in pediatric acute lymphoblastic leukemia by disrupting 3D chromatin organization

| PRJNA821457 | ENA