Evidence map›Paper›PMID 39215060›Full record

ArticleLeukemia2024

IL-10R inhibition reprograms tumor-associated macrophages and reverses drug resistance in multiple myeloma.

Jennifer Sun, Stefan Corradini, Feda Azab, Monica Shokeen, Barbara Muz, Katerina E Miari, Mina Maksimos, Camila Diedrich, Obed Asare, Kinan Alhallak and 13 more

Abstract read
In one paragraph

Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Review
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  11. Article
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  13. SSTNSignal transduction and targeted therapy · 2026
    Article
  14. Article
  15. Emerging roles of RNA mInternational journal of oncology · 2026
    Review
  16. Review
  17. FAPαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  18. Article
  19. Article
  20. Article
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

23 authors.

Jennifer SunDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Stefan CorradiniCharles Oakley Laboratories, Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, UK.ORCID 0000-0002-5990-806X
Feda AzabDepartment of Biomedical Engineering, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Monica ShokeenDepartment of Biomedical Engineering, Washington University in St. Louis McKelvey School of Engineering, St. Louis, MO, USA.
Barbara MuzDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Katerina E MiariCharles Oakley Laboratories, Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, UK.ORCID 0000-0003-3008-966X
Mina MaksimosDepartment of Biomedical Engineering, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Camila DiedrichDepartment of Biomedical Engineering, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Obed AsareDepartment of Biomedical Engineering, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kinan AlhallakDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Chaelee ParkDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID 0000-0002-3909-0096
Berit LubbenDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Yixuan ChenDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID 0000-0001-7496-9648
Ola AdebayoDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Hannah BashDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Sarah KelleyDepartment of Medicine, Oncology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Mark FialaDepartment of Medicine, Oncology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID 0000-0002-0208-5023
Diane E BenderAlvin J. Siteman Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital, St. Louis, MO, USA.ORCID 0000-0002-8311-4390
Haibin ZhouDepartment of Internal Medicine University of Michigan, Ann Arbor, Michigan, USA.
Shaomeng WangDepartment of Internal Medicine University of Michigan, Ann Arbor, Michigan, USA.
Ravi VijAlvin J. Siteman Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital, St. Louis, MO, USA.
Mark T S WilliamsCharles Oakley Laboratories, Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, UK.ORCID 0000-0003-1114-1418
Abdel Kareem AzabDepartment of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. abdelkareem.azab@utsouthwestern.edu.ORCID 0000-0002-6371-2780

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Cancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas) RR220088NCI NIH HHS P30 CA091842
6 · The paper itself

Abstract

Multiple myeloma (MM) is the cancer of plasma cells within the bone marrow and remains incurable. Tumor-associated macrophages (TAMs) within the tumor microenvironment often display a pro-tumor phenotype and correlate with tumor proliferation, survival, and therapy resistance. IL-10 is a key immunosuppressive cytokine that leads to recruitment and development of TAMs. In this study, we investigated the role of IL-10 in MM TAM development as well as the therapeutic application of IL-10/IL-10R/STAT3 signaling inhibition. We demonstrated that IL-10 is overexpressed in MM BM and mediates M2-like polarization of TAMs in patient BM, 3D co-cultures in vitro, and mouse models. In turn, TAMs promote MM proliferation and drug resistance, both in vitro and in vivo. Moreover, inhibition of IL-10/IL-10R/STAT3 axis using a blocking IL-10R monoclonal antibody and STAT3 protein degrader/PROTAC prevented M2 polarization of TAMs and the consequent TAM-induced proliferation of MM, and re-sensitized MM to therapy, in vitro and in vivo. Therefore, our findings suggest that inhibition of IL-10/IL-10R/STAT3 axis is a novel therapeutic strategy with monotherapy efficacy and can be further combined with current anti-MM therapy, such as immunomodulatory drugs, to overcome drug resistance. Future investigation is warranted to evaluate the potential of such therapy in MM patients.

Indexed as

Drug Resistance, NeoplasmInterleukin-10Multiple MyelomaReceptors, Interleukin-10STAT3 Transcription FactorTumor-Associated MacrophagesTumor MicroenvironmentAnimalsCell Line, TumorCell ProliferationHumansMiceSignal TransductionIL10 protein, humanInterleukin-10Receptors, Interleukin-10STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID39215060
PMCPMC11518999

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.