Evidence map›Paper›PMID 23432691›Full record

ReviewLeukemia & lymphoma2013

Macrophages in multiple myeloma: emerging concepts and therapeutic implications.

Fotis Asimakopoulos, Jaehyup Kim, Ryan A Denu, Chelsea Hope, Jeffrey L Jensen, Samuel J Ollar, Ellen Hebron, Claire Flanagan, Natalie Callander, Peiman Hematti

Abstract readReview
In one paragraph

Review in Leukemia & lymphoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  16. Tumor-Associated Macrophages in Osteosarcoma: From Mechanisms to Therapy.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Review
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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

10 authors at 2 institutions in 1 country.

Fotis AsimakopoulosDivision of Hematology/Oncology, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health , Madison, WI , USA and University of Wisconsin Carbone Cancer Center , Madison, WI , USA.
Jaehyup Kim
Ryan A Denu
Chelsea Hope
Jeffrey L Jensen
Samuel J Ollar
Ellen Hebron
Claire Flanagan
Natalie Callander
Peiman Hematti
University of Wisconsin–Madison · USUniversity of Wisconsin Carbone Cancer Center · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
INTEGRATED TRAINING FOR PHYSICIAN-SCIENTISTST32GM008692 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E · 1998 to 2020
$10.3M
RESEARCH TRAINING IN HEMATOLOGYT32HL007899 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Jane Ellen Churpek · 1998 to 2026
$8.2M
Institutional Clinical and Translational Science AwardTL1TR000429 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$1.5M
Institutional Clinical and Translational Science Award (UW-Madison)(TL1)TL1RR025013 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$1.1M
NCATS NIH HHS 9U54TR000021NCATS NIH HHS TL1 TR000429NCATS NIH HHS UL1 TR000427NCI NIH HHS P30 CA014520NCRR NIH HHS TL1 RR025013NHLBI NIH HHS T32 HL007899NIGMS NIH HHS T32 GM008692
6 · The paper itself

Abstract

Multiple myeloma, a clonal plasma cell malignancy, has long provided a prototypic model to study regulatory interactions between malignant cells and their microenvironment. Myeloma-associated macrophages have historically received limited scrutiny, but recent work points to central and non-redundant roles in myeloma niche homeostasis. The evidence supports a paradigm of complex, dynamic and often mutable interactions between macrophages and other cellular constituents of the niche. We and others have shown that macrophages support myeloma cell growth, viability and drug resistance through both contact-mediated and non-contact-mediated mechanisms. These tumor-beneficial roles have evolved in opposition to, or in parallel with, intrinsic pro-inflammatory and tumoricidal properties. Thus, simple blockade of protective "don't eat me" signals on the surface of myeloma cells leads to macrophage-mediated myeloma cell killing. Macrophages also enhance the tumor-supportive role of mesenchymal stem/stromal cells (MSCs) in the niche: importantly, this interaction is bidirectional, producing a distinct state of macrophage polarization that we termed "MSC-educated macrophages." The intriguing pattern of cross-talk between macrophages, MSCs and tumor cells highlights the myeloma niche as a dynamic multi-cellular structure. Targeted reprogramming of these interactions harbors significant untapped therapeutic potential, particularly in the setting of minimal residual disease, the main obstacle toward a cure.

Indexed as

AnimalsCell CommunicationCell SurvivalHumansImmunotherapyMacrophage ActivationMacrophagesMAP Kinase Kinase KinasesMesenchymal Stem CellsMultiple MyelomaNeovascularization, PathologicPhenotypeProto-Oncogene ProteinsTumor MicroenvironmentMAP3K8 protein, humanMAP Kinase Kinase KinasesProto-Oncogene Proteins

Identifiers

PMID23432691
PMCPMC3686978
OpenAlexW2051230418

What OpenQuestion holds

Textmetadata
LicenceTDM
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.