Evidence map›Paper›PMID 34007044›Full record

ArticleLeukemia2021

JunB is a key regulator of multiple myeloma bone marrow angiogenesis.

Fengjuan Fan, Stefano Malvestiti, Sonia Vallet, Judith Lind, Jose Manuel Garcia-Manteiga, Eugenio Morelli, Qinyue Jiang, Anja Seckinger, Dirk Hose, Hartmut Goldschmidt and 12 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 11 institutions in 6 countries.

Fengjuan FanInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0001-8727-5258
Stefano MalvestitiDepartment of Medical Oncology, National Center for Tumor Diseases (NCT), University of Heidelberg, Heidelberg, Germany.
Sonia ValletDepartment of Internal Medicine II, University Hospital Krems, Krems an der Donau, Austria.
Judith LindMolecular Oncology and Hematology Unit, Karl Landsteiner University of Health Sciences, Krems an der Donau, Austria.
Jose Manuel Garcia-ManteigaCenter for Translational Genomics and Bioinformatics, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Eugenio MorelliDepartment of Experimental and Clinical Medicine, University "Magna Græcia" of Catanzaro, Catanzaro, Italy.ORCID http://orcid.org/0000-0002-8850-0442
Qinyue JiangInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Anja SeckingerUniversity Hospital Heidelberg, Heidelberg, Germany.
Dirk HoseUniversity Hospital Heidelberg, Heidelberg, Germany.
Hartmut GoldschmidtDepartment of Medical Oncology, National Center for Tumor Diseases (NCT), University of Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-0961-0035
Andreas StadlbauerDepartment of Neurosurgery, Friedrich-Alexander University (FAU) Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0001-8348-2620
Chunyan SunInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Heng MeiInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0001-7941-2443
Martin PecherstorferDepartment of Internal Medicine II, University Hospital Krems, Krems an der Donau, Austria.
Latifa BakiriGenes & Disease Group, Department of Dermatology, Medical University of Vienna (MUW), Vienna, Austria.ORCID http://orcid.org/0000-0002-6300-2420
Erwin F WagnerGenes & Disease Group, Department of Dermatology, Medical University of Vienna (MUW), Vienna, Austria.ORCID http://orcid.org/0000-0001-7872-0196
Giovanni TononCenter for Translational Genomics and Bioinformatics, IRCCS San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0003-2973-5038
Martin SattlerDepartment of Medicine, Harvard Medical School, Boston, MA, USA.
Yu HuInstitute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. dr_huyu@126.com.ORCID http://orcid.org/0000-0002-2815-4568
Pierfrancesco TassoneDepartment of Experimental and Clinical Medicine, University "Magna Græcia" of Catanzaro, Catanzaro, Italy.
Dirk JaegerDepartment of Medical Oncology, National Center for Tumor Diseases (NCT), University of Heidelberg, Heidelberg, Germany.
Klaus PodarDepartment of Medical Oncology, National Center for Tumor Diseases (NCT), University of Heidelberg, Heidelberg, Germany. klaus.podar@krems.lknoe.at.ORCID http://orcid.org/0000-0002-7414-3632
Union Hospital · CNHeidelberg University · DEMedical University of Vienna · ATUniversitätsklinikum Krems · ATVita-Salute San Raffaele University · ITVrije Universiteit Brussel · BEBrigham and Women's Hospital · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHarvard University · USKarl Landsteiner University of Health Sciences · ATMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow (BM) angiogenesis significantly influences disease progression in multiple myeloma (MM) patients and correlates with adverse prognosis. The present study shows a statistically significant correlation of the AP-1 family member JunB with VEGF, VEGFB, and IGF1 expression levels in MM. In contrast to the angiogenic master regulator Hif-1α, JunB protein levels were independent of hypoxia. Results in tumor-cell models that allow the induction of JunB knockdown or JunB activation, respectively, corroborated the functional role of JunB in the production and secretion of these angiogenic factors (AFs). Consequently, conditioned media derived from MM cells after JunB knockdown or JunB activation either inhibited or stimulated in vitro angiogenesis. The impact of JunB on MM BM angiogenesis was finally confirmed in a dynamic 3D model of the BM microenvironment, a xenograft mouse model as well as in patient-derived BM sections. In summary, in continuation of our previous study (Fan et al., 2017), the present report reveals for the first time that JunB is not only a mediator of MM cell survival, proliferation, and drug resistance, but also a promoter of AF transcription and consequently of MM BM angiogenesis. Our results thereby underscore worldwide efforts to target AP-1 transcription factors such as JunB as a promising strategy in MM therapy.

Indexed as

AnimalsBone MarrowCell Line, TumorFemaleHeterograftsHumansInsulin-Like Growth Factor IInterleukin-6MiceMice, Inbred NODMice, SCIDMultiple MyelomaNeovascularization, PathologicPrimary Cell CultureTranscription FactorsVascular Endothelial Growth Factor AIGF1 protein, humanIL6 protein, humanInsulin-Like Growth Factor IInterleukin-6JunB protein, humanTranscription FactorsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor BVEGFA protein, humanVEGFB protein, human

Identifiers

PMID34007044
PMCPMC8632680
OpenAlexW3160482846

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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.