Evidence map›Paper›PMID 26556857›Full record

ArticleOncotarget2015

The bone marrow microenvironment enhances multiple myeloma progression by exosome-mediated activation of myeloid-derived suppressor cells.

Jinheng Wang, Kim De Veirman, Nathan De Beule, Ken Maes, Elke De Bruyne, Els Van Valckenborgh, Karin Vanderkerken, Eline Menu

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

114 citing papers in PubMed.

  1. Review
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  5. Immunoregulatory extracellular vesicles in multiple myeloma patients' peripheral blood.Extracellular vesicles and circulating nucleic acids · 2026
    Article
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54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jinheng WangDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Kim De VeirmanDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Nathan De BeuleDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Ken MaesDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Elke De BruyneDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Els Van ValckenborghDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Karin VanderkerkenDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.
Eline MenuDepartment of Hematology and Immunology, Myeloma Center Brussels, Vrije Universiteit Brussels (VUB), Brussels, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes, extracellular nanovesicles secreted by various cell types, modulate the bone marrow (BM) microenvironment by regulating angiogenesis, cytokine release, immune response, inflammation, and metastasis. Interactions between bone marrow stromal cells (BMSCs) and multiple myeloma (MM) cells play crucial roles in MM development. We previously reported that BMSC-derived exosomes directly promote MM cell growth, whereas the other possible mechanisms for supporting MM progression by these exosomes are still not clear. Here, we investigated the effect of BMSC-derived exosomes on the MM BM cells with specific emphasis on myeloid-derived suppressor cells (MDSCs). BMSC-derived exosomes were able to be taken up by MM MDSCs and induced their expansion in vitro. Moreover, these exosomes directly induced the survival of MDSCs through activating STAT3 and STAT1 pathways and increasing the anti-apoptotic proteins Bcl-xL and Mcl-1. Inhibition of these pathways blocked the enhancement of MDSC survival. Furthermore, these exosomes increased the nitric oxide release from MM MDSCs and enhanced their suppressive activity on T cells. Taken together, our results demonstrate that BMSC-derived exosomes activate MDSCs in the BM through STAT3 and STAT1 pathways, leading to increased immunosuppression which favors MM progression.

Indexed as

AnimalsBlotting, WesternBone MarrowCell SeparationDisease ProgressionExosomesFemaleFlow CytometryImmune ToleranceMesenchymal Stem CellsMiceMice, Inbred C57BLMultiple MyelomaMyeloid CellsTumor Microenvironmentbone marrow stromal cellsexosomesimmunosuppressionmultiple myelomamyeloid-derived suppressor cells

Identifiers

PMID26556857
PMCPMC4791281

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.