Evidence map›Paper›PMID 41463400›Full record

ArticleBiomolecules2025

Humanized Bone Model Identifies BMP6 as a Multifunctional Regulator in Myeloma Bone Disease.

Jiaxian Wang, Thomas Baardemans, Ricardo de Matos Simoes, Willy Noort, Ruud W J Ruiter, Henk-Jan Prins, Susan E van Hal-van Veen, Huipin Yuan, Joost D de Bruijn, Anton C M Martens and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Jiaxian WangDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Thomas BaardemansDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.ORCID 0009-0005-1500-6688
Ricardo de Matos SimoesDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Willy NoortDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Ruud W J RuiterDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Henk-Jan PrinsDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Susan E van Hal-van VeenDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Huipin YuanKuros Biosciences BV, 3723 MB Bilthoven, The Netherlands.
Joost D de BruijnKuros Biosciences BV, 3723 MB Bilthoven, The Netherlands.
Anton C M MartensDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Constantine S MitsiadesDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Sonja ZweegmanDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Maria ThemeliDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.
Richard W J GroenDepartment of Hematology, Amsterdam UMC, VU University Medical Center, Cancer Center Amsterdam, 1081 HV Amsterdam, The Netherlands.ORCID 0000-0002-5010-4604

Funding

Dutch Cancer Society 13923Dutch Cancer Society VU2011-5127
6 · The paper itself

Abstract

Multiple myeloma (MM) is a plasma cell malignancy that disrupts bone homeostasis by suppressing osteogenesis and promoting osteoclast activity. While most therapeutic interventions to date have focused on targeting tumor cells and reducing osteolysis, we investigate whether osteoinductive strategies can restore bone formation and counteract disease progression. Using a human bone marrow-like scaffold model that enables direct in vivo evaluation of tumor-stroma interactions and human bone formation, we demonstrate that MM-derived mesenchymal stromal cells (MSCs) retain osteogenic potential but are functionally suppressed by MM cells. Transcriptomic profiling of MM-primed MSCs revealed the downregulation of small leucine-rich proteoglycans (SLRPs),

Indexed as

Bone DiseasesBone Morphogenetic Protein 6Multiple MyelomaAnimalsCell DifferentiationCell Line, TumorCell ProliferationHumansMesenchymal Stem CellsMiceOsteogenesisBMP6 protein, humanBone Morphogenetic Protein 6BMPbone diseasemultiple myelomaosteoblastxenograft

Identifiers

PMID41463400
PMCPMC12731031

What OpenQuestion holds

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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.