Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of VK12653 Multiple Myeloma bone marrow microenvironmentupon treatment with anti-CD137 agonists

ABSTRACT: We report the RNA sequencing of VK12653 Multiple Myeloma bone marrow microenvironment upon treatment with anti-CD137 agonists

ORGANISM(S): Mus musculus

PROVIDER: GSE206545 | GEO | 2023/06/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single cell Transcriptomic analysis of CD8+ T cells treated with anti-CD137 agonists within VK12653 Multiple Myeloma bone marrow microenvironment .

Project description:We report the single cell RNA sequencing of mouse CD8+ T cells infiltrating VK12653 Multiple Myeloma lesions upon treatment with anti-CD137 agonists .

2023-06-30 | GSE205702 | GEO

Transcriptomic analysis of VK12653 Multiple Myeloma bone marrow microenvironmentupon treatment with anti-CD137 agonists

Project description:Transcriptomic analysis of VK12653 Multiple Myeloma bone marrow microenvironmentupon treatment with anti-CD137 agonists

| PRJNA851353 | ENA

Single cell Transcriptomic analysis of CD8+ T cells treated with anti-CD137 agonists within VK12653 Multiple Myeloma bone marrow microenvironment .

Project description:Single cell Transcriptomic analysis of CD8+ T cells treated with anti-CD137 agonists within VK12653 Multiple Myeloma bone marrow microenvironment .

| PRJNA847213 | ENA

CD137 (4-1BB) requires physically associated cIAPs for signal transduction and antitumor effects

Project description:CD137 (4-1BB) is a member of the TNFR family that mediates potent T-cell costimulatory signals upon ligation by CD137L or agonist monoclonal antibodies. CD137 agonists attain immunotherapeutic antitumor effects in cancer mouse models and multiple agents of this kind are undergoing clinical trials. We show that cIAP1 and cIAP2 are physically associated with the CD137-signaling complex. Moreover, cIAPs are required for CD137 signaling towards the NF-κB and MAPK pathways and for costimulation of human and mouse T lymphocytes. Functional evidence was substantiated with SMAC-mimetics that trigger cIAPs degradation and by transfecting cIAP dominant-negative variants. Antitumor effects of agonist anti-CD137 mAbs are critically dependent on the integrity of cIAPs in cancer mouse models and cIAPs are also required for signaling from CARs encompassing CD137’s cytoplasmic tail.

2024-05-24 | PXD042585 | Pride

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

Inhibition of microRNA-138 enhances bone formation in multiple myeloma bone marrow niche

Project description:Myeloma bone disease is a devastating complication of multiple myeloma (MM) and is caused by dysregulation of bone remodeling processes in the bone marrow microenvironment. Previous studies showed that microRNA-138 (miR-138) is a negative regulator of osteogenic differentiation of mesenchymal stromal cells (MSCs) and that inhibiting its function enhances bone formation in vitro. In this study, we explored the role of miR-138 in myeloma bone disease and evaluated the potential of systemically delivered locked nucleic acid (LNA)-modified anti-miR-138 oligonucleotides in suppressing myeloma bone disease. We showed that expression of miR-138 was significantly increased in MSCs from MM patients (MM-MSCs) and myeloma cells compared to those from healthy subjects. Furthermore, inhibition of miR-138 resulted in enhanced osteogenic differentiation of MM-MSCs in vitro and increased number of endosteal osteoblastic lineage cells (OBCs) and bone formation rate in mouse models of myeloma bone disease. RNA sequencing of the OBCs identified TRPS1 and SULF2 as potential miR-138 targets that were de-repressed in anti-miR-138 treated mice. In summary, these data indicate that inhibition of miR-138 enhances bone formation in MM and that pharmacological inhibition of miR-138 could represent a new therapeutic strategy for treatment of myeloma bone disease.

2018-06-01 | GSE111651 | GEO

microRNA profiling of multiple myeloma bone marrow

Project description:Bone marrow microenvironment in MM contains a unique miR signature, which is partially present and detectable in the peripheral blood. A subset of miRs (let-7i, miR-106b, miR-15a, and miR16) shows aberrant expression in the precursor lesion of MGUS, while aberrant expression of other miRs (let-7a, miR-15a/b, miR-19b, miR-20a, miR-21, miR-223, and miR-361) is associated with cell proliferation and disease progression. miRNA profiling was performed using Agilent miRNA array platforms with RNAs isolated from the bone marrow supernatant of multiple myeloma.

2016-07-01 | E-GEOD-49261 | biostudies-arrayexpress

Bone marrow neutrophils regulate multiple myeloma by releasing DNA

Project description:Development of Multiple Myeloma is associated with an accumulation of myeloid derived suppressor cells (MDSCs ) - cells that are morphologically and phenotypically similar to neutrophils (PMN-MDSC) and monocytes (M-MDSC), but are distinct in their functional and biochemical characteristics as well as in their ability to suppress immune responses. In our study, we found that both neutrophils and PMN-MDSCs equally promoted MM survival and decreased MM cell sensitivity to chemotherapy. Therefore, we used a microarray to elucidate the mechanism of the protective effect of neutrophils on myeloma cells.

2018-08-31 | GSE69834 | GEO

Single cell Transcriptomic analysis of CD8+ T cells from bone marrow chimeras reconstituted with CD137 wild-type or knock out bone marrow, and implanted with B16K1 melanoma.

Project description:We report the single cell RNA sequencing of mouse CD8+ T cells in bone marrow chimeras reconsitituted with equal amounts of CD137-/-tomato+ and CD137-/-tomato- bone marrow implanted with B16K1 melanoma. CD8 T cells from the spleen or the tumor infiltrate are compared.

2023-06-30 | GSE205703 | GEO

Repurposing tofacitinib as an anti-myeloma therapeutic to reverse growth-promoting effects of the bone marrow microenvironment

Project description:The myeloma bone marrow microenvironment drives proliferation of malignant plasma cells and promotes resistance to therapy. Interleukin-6 (IL-6) and downstream JAK/STAT signaling are thought to be central components of these microenvironment-induced phenotypes. In a prior drug repurposing screen, we identified tofacitinib, a pan-JAK inhibitor FDA-approved for rheumatoid arthritis, as an agent that may reverse the tumor-stimulating effects of bone marrow mesenchymal stromal cells.Here, we validated both in vitro, in stromal-responsive human myeloma cell lines, and in vivo, in orthotopic disseminated murine xenograft models of myeloma, that tofacitinib showed both single-agent and combination therapeutic efficacy in myeloma models. Surprisingly, we found that ruxolitinib, an FDA-approved agent targeting JAK1 and JAK2, did not lead to the same anti-myeloma effects. Combination with a novel irreversible JAK3-selective inhibitor also did not rescue ruxolitinib effects. RNA-seq and unbiased phosphoproteomics revealed that marrow stromal cells drive a JAK/STAT-mediated proliferative program in myeloma plasma cells, and tofacitinib reversed the large majority of these pro-growth signals. Taken together, our results suggest that tofacitinib specifically reverses the growth-promoting effects of the tumor microenvironment through blocking an IL-6-mediated signaling axis. As tofacitinib is already FDA-approved, these results can be rapidly translated into potential clinical benefits for myeloma patients.

2018-10-24 | PXD006581 | Pride

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