Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigation of bone marrow microenvironment-induced drug resistance in acute lymphoblastic leukemia (ALL)

ABSTRACT: Investigation of bone marrow microenvironment-induced drug resistance in acute lymphoblastic leukemia (ALL)

PROVIDER: PRJNA822779 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional response in acute lymphoblastic leukaemia cells to bone marrow microenvironment

Project description:Glucocorticoids (GCs) and topoisomerase II inhibitors are used in the treatment of acute lymphoblastic leukaemia (ALL) due to their ability to induce cell death in lymphoid cells. GC-induced apoptosis is mediated by the glucocorticoid receptor (GR), whereas topoisomerase II inhibitors cause DNA damage and activate sensors of DNA damage including the tumour suppressor p53. In order to shed light on the role of the microenvironment in cell death and identify determinants of drug sensitivity we performed transcriptomic analysis in ALL cells treated with the synthetic glucocorticoid dexamethasone, and the topoisomerase II inhibitor etoposide combined with bone marrow-derived conditioned media (CM).

2017-08-30 | E-MTAB-4761 | biostudies-arrayexpress

The bone marrow microenvironment of pre-B acute lymphoblastic leukemia at single-cell resolution

Project description:The bone marrow microenvironment of leukemia plays a key role in leukemia progression, but its molecular complexity in pre-B acute lymphoblastic leukemia (B-ALL), the most common cancer in children, remains poorly understood. Here we use single-cell RNA sequencing to characterise the bone marrow microenvironment during B-ALL progression.

2020-07-27 | GSE148115 | GEO

Investigation of bone marrow microenvironment-induced drug resistance in acute lymphoblastic leukemia (ALL)

Project description:Bulk RNA-seq of B-ALL cells cocultured with bone marrow-mesenchymal stem cells (BM-MSC) identified that B-ALL acquire epithelial-mesenchymal transition (EMT) properties by interacting with primary bone marrow-mesenchymal stem cells (BM-MSC) and scRNA-seq dissected the hybrid cluster of adherent B-ALL (Adh B-ALL) harboring B-ALL and BM-MSC features induced by EMT program

2022-05-31 | GSE200039 | GEO

Bone marrow microenvironment mediated drug resistance in Acute promyelocytic leukemia

Project description:Bone marrow microenvironment mediated drug resistance in Acute promyelocytic leukemia

| PRJNA514741 | ENA

The Evolving Immune Microenvironment of B-cell Acute Lymphoblastic Leukemia [human bone marrow dataset]

Project description:The Evolving Immune Microenvironment of B-cell Acute Lymphoblastic Leukemia [human bone marrow dataset]

| PRJNA533995 | ENA

The bone marrow microenvironment of pre-B acute lymphoblastic leukemia at single-cell resolution

Project description:The bone marrow microenvironment of pre-B acute lymphoblastic leukemia at single-cell resolution

| PRJNA623280 | ENA

RNA-seq of primary human bone marrow derived mesenchymal stromal cells from pediatric B-cell acute lymphoblastic leukemia (B-ALL) patients

Project description:To investigate the identity of the tumor microenvironment in acute lymphoblastic leukemia (B-ALL), the transcriptome of mesenchymal stromal cells derived from bone marrow of three pediatric patients at the onset of the disease was analyzed and compared with its normal counterpart.

2021-10-16 | E-MTAB-10838 | biostudies-arrayexpress

Bone Marrow Microenvironment Niche Regulates miR-221/222 in Acute Lymphoblastic Leukemia.

Project description: Not available

| S-EPMC5065748 | biostudies-literature

Bone marrow microenvironment mediated drug resistance in Acute promyelocytic leukemia

Project description:About 5-10% newly diagnosed and about 20-30% of relapsed acute promyelocytic leukemia (APL) patients will have disease recurrence after receiving currently accepted standards of care. While there are reports of micro-environment mediated drug resistance (EM-DR) in AML, there is no data on the effect of malignant promyelocyte and stromal interaction on Arsenic trioxide (ATO) induced apoptosis. There are limited study available on the effect of leukemic cell interaction on stromal cells. We undertook a preliminary study to evaluate the changes induced by leukemic cells on stromal cells. In a gene expression profiling comparing HS-5 cells in co-culture with NB4 cells alone, 8456 genes were differentially regulated. On a preliminary analysis, we observed an up-regulation of various pathways such as adhesion, Cytokines, Wnt signalling in the stromal cells.

2020-01-10 | GSE124987 | GEO

Multiple myeloma-derived extracellular vesicles modulate the bone marrow immune microenvironment

Project description:One of the hallmarks of multiple myeloma (MM) is a permissive BM microenvironment. Increasing evidence suggest that cell-to-cell communication between myeloma and immune cells via tumor cell-derived extracellular vesicles (EV) plays a key role in the pathogenesis of MM. Hence, we aimed to explore BM immune alterations induced by MM-derived EV. For this, we inoculated immunocompetent BALB/cByJ mice with a myeloma cell line - MOPC315.BM -, inducing a MM phenotype. Upon tumor establishment, characterization of the BM microenvironment revealed the expression of both activation and suppressive markers by lymphocytes, such as Granzyme b and PD-1, respectively. In addition, conditioning of the animals with MOPC315.BM-derived EV, before transplantation of the MOPC315.BM tumor cells, did not anticipate the disease phenotype. However, it induced features of suppression in the BM milieu, such as an increase in PD-1 expression by CD4+ T cells. Overall, our findings reveal the involvement of MOPC315.BM-derived EV protein content as promoters of immune niche remodeling, strengthening the importance of assessing the mechanisms by which MM may impact the immune microenvironment.

2022-07-05 | PXD032934 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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