Evidence map›Paper›PMID 29296919›Full record

ArticleBlood advances2017

Hypoxia promotes IL-32 expression in myeloma cells, and high expression is associated with poor survival and bone loss.

Muhammad Zahoor, Marita Westhrin, Kristin Roseth Aass, Siv Helen Moen, Kristine Misund, Katarzyna Maria Psonka-Antonczyk, Mariaserena Giliberto, Glenn Buene, Anders Sundan, Anders Waage and 2 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

37 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

12 authors at 3 institutions in 2 countries.

Muhammad ZahoorCentre of Molecular Inflammation Research and.
Marita WesthrinDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0001-6932-2102
Kristin Roseth AassCentre of Molecular Inflammation Research and.
Siv Helen MoenDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Kristine MisundDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Katarzyna Maria Psonka-AntonczykBiophysics and Medical Technology, Department of Physics, Norwegian University of Science and Technology, Trondheim, Norway.
Mariaserena GilibertoCentre of Molecular Inflammation Research and.
Glenn BueneDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Anders SundanCentre of Molecular Inflammation Research and.
Anders WaageDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Anne-Marit SponaasDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Therese StandalCentre of Molecular Inflammation Research and.ORCID 0000-0003-3314-8522
Norwegian University of Science and Technology · NOCentre for Inflammation Research · GBSt Olav's University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematologic cancer characterized by expansion of malignant plasma cells in the bone marrow. Most patients develop an osteolytic bone disease, largely caused by increased osteoclastogenesis. The myeloma bone marrow is hypoxic, and hypoxia may contribute to MM disease progression, including bone loss. Here we identified interleukin-32 (IL-32) as a novel inflammatory cytokine expressed by a subset of primary MM cells and MM cell lines. We found that high IL-32 gene expression in plasma cells correlated with inferior survival in MM and that IL-32 gene expression was higher in patients with bone disease compared with those without. IL-32 was secreted from MM cells in extracellular vesicles (EVs), and those EVs, as well as recombinant human IL-32, promoted osteoclast differentiation both in vitro and in vivo. The osteoclast-promoting activity of the EVs was IL-32 dependent. Hypoxia increased plasma-cell IL-32 messenger RNA and protein levels in a hypoxia-inducible factor 1α-dependent manner, and high expression of IL-32 was associated with a hypoxic signature in patient samples, suggesting that hypoxia may promote expression of IL-32 in MM cells. Taken together, our results indicate that targeting IL-32 might be beneficial in the treatment of MM bone disease in a subset of patients.

Identifiers

PMID29296919
PMCPMC5745138
OpenAlexW2772904315

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.