Evidence map›Paper›PMID 30408155›Full record

Trial reportBritish journal of haematology2019

Mesenchymal stem cells gene signature in high-risk myeloma bone marrow linked to suppression of distinct IGFBP2-expressing small adipocytes.

Syed J Mehdi, Sarah K Johnson, Joshua Epstein, Maurizio Zangari, Pingping Qu, Antje Hoering, Frits van Rhee, Carolina Schinke, Sharmilan Thanendrarajan, Bart Barlogie and 3 more

Open access · bronzeAbstract readMulticenter StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in British journal of haematology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
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

18 citing papers in PubMed, 22 citations in OpenAlex.

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  16. Gene: X · 2020
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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

13 authors at 2 institutions in 1 country.

Syed J MehdiMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Sarah K JohnsonMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Joshua EpsteinMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Maurizio ZangariMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.ORCID 0000-0002-1720-3854
Pingping QuCancer Research and Biostatistics, Seattle, WA, USA.
Antje HoeringCancer Research and Biostatistics, Seattle, WA, USA.
Frits van RheeMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Carolina SchinkeMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Sharmilan ThanendrarajanMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Bart BarlogieMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Faith E DaviesMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Gareth J MorganMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
Shmuel YaccobyMyeloma Institute, University of Arkansas for Medical Sciences, Little Rock, AR, USA.ORCID 0000-0003-1823-3411
University of Arkansas for Medical Sciences · USCancer Research And Biostatistics · US

Funding

Tumor Cell-Microenvironment Interactions in the Molecular Pathogenesis of MultiplP01CA055819 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI YACCOBY, SHMUEL · 1993 to 2013
$49.7M
NCI NIH HHS P01 CA055819
6 · The paper itself

Abstract

Recent studies suggest that multiple myeloma (MM) induces proliferation and expansion of bone marrow (BM) mesenchymal stem cells (MSCs), but others showed that MM cells induce MSC senescence. To clarify the interaction between MM and MSCs, we exploited our established MSC gene signature to identify gene expression changes in myeloma MSCs and associated functional differences. Single MSCs from patients with MM had changes in expression of genes associated with cellular proliferation and senescence and a higher proportion of senescent cells and lower proliferative potential than those from age-matched healthy donors. Single MSCs from both sources heterogeneously express MSC genes associated with adipogenesis and osteoblastogenesis. We identified the gene encoding insulin-like growth factor-binding protein 2 (IGFBP2), an MSC gene commonly altered in high risk MM, as under-expressed. Morphologically, IGFBP2+ cells are underrepresented in MM BM compared to smouldering MM. Strong IGFBP2 and adiponectin co-expression was detected in a subset of small adipocytes. Co-culturing normal MSCs with myeloma cells suppressed MSC differentiation to adipocytes and osteoblasts, and reduced expression of IGFBP2 and adiponectin. Recombinant IGFBP2 blocked IGF1-mediated myeloma cell growth. Our data demonstrate that myeloma MSCs are less proliferative and that IGFBP2+ small adipocytes are a distinct mesenchymal cell population suppressed by myeloma.

Indexed as

AdipocytesBone MarrowGene Expression Regulation, NeoplasticMesenchymal Stem CellsMultiple MyelomaCell DifferentiationFemaleHumansInsulin-Like Growth Factor Binding Protein 2MaleNeoplasm ProteinsRisk FactorsIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Neoplasm Proteinsadipocytesbone marrowIGFBP2microenvironmentmyeloma

Identifiers

PMID30408155
PMCPMC6361704
OpenAlexW2900415496

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.