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Cells
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Novel Insights into Molecular Mechanisms and Therapy of Myeloma
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Novel Insights into Molecular Mechanisms and Therapy of Myeloma

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 5 October 2025 | Viewed by 1527

Special Issue Editors

Prof. Dr. Yusuke Furukawa

E-Mail Website
Guest Editor
Center for Medical Education, Teikyo University of Science, 2-2-1 Senjyu-sakuragi, Adachi, Tokyo 1120-0045, Japan
Interests: multiple myeloma; malignant lymphoma; cancer stem cell; epigenetics; drug resistance; autophagy
Dr. Jian Wu

E-Mail Website
Guest Editor
Duke University Medical Center, 905 S Lasalle St, Durham, NC 27710, USA
Interests: multiple myeloma; drug resistance; CAR-T; molecular pathway; stem cell; radiation protection; chemo protection; novel target

Special Issue Information

Dear Colleagues,

Multiple myeloma (MM) is a clonal plasma cell malignancy. It is the second most common hematologic malignancy in the United States. Although current anti-myeloma agents, such as immunomodulatory agents, proteasome inhibitors, and monoclonal antibodies, have significantly improved the outcomes of MM patients, MM remains to be an incurable disease with high rates of drug resistance and relapse. A better understanding of the genomic landscape of MM could help clinicians develop more tailored therapy for patients.

Recent advances in genetic and cellular technologies, in combination with diverse treatment approaches, have significantly improved our knowledge on MM.

Collectively, the original research and review articles in this Special Issue cover important aspects of biomedical research. They provide new insights into the molecular mechanisms underlying multiple myeloma and identify novel diagnostic and prognostic biomarkers in various models. This Special Issue focuses on emerging molecular discoveries and approaches, emphasizing the significance of understanding molecular mechanisms in multiple myeloma for the development of novel diagnostic and therapeutic tools.

Prof. Dr. Yusuke Furukawa
Dr. Jian Wu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • multiple myeloma
  • CAR-T therapy
  • relapse
  • methylation
  • drug resistance
  • treatment strategy
  • molecular mechanism
  • novel target
  • biomarker

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Published Papers (2 papers)

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16 pages, 2561 KiB  
Article
β-Arrestin 2 as a Prognostic Indicator and Immunomodulatory Factor in Multiple Myeloma
by Parker Mathews, Xiaobei Wang, Jian Wu, Shaima Jabbar, Kimberly Burcher, Lindsay Rein and Yubin Kang
Cells 2025, 14(7), 496; https://doi.org/10.3390/cells14070496 - 26 Mar 2025
Viewed by 442
Abstract
β-arrestin 2 (ARRB2) is involved in the desensitization and trafficking of G protein-coupled receptors (GPCRs) and plays a critical role in cell proliferation, apoptosis, chemotaxis, and immune response modulation. The role of ARRB2 in the pathogenesis of multiple myeloma (MM) has not been [...] Read more.
β-arrestin 2 (ARRB2) is involved in the desensitization and trafficking of G protein-coupled receptors (GPCRs) and plays a critical role in cell proliferation, apoptosis, chemotaxis, and immune response modulation. The role of ARRB2 in the pathogenesis of multiple myeloma (MM) has not been elucidated. This study addressed this question by evaluating the expression of ARRB2 in bone marrow (BM) samples from newly diagnosed MM patients and deriving correlations with key clinical outcomes. In light of recent trends towards the use of immune checkpoint inhibitors across malignancies, the effect of ARRB2 in the regulation of the PD-1/PD-L1 axis was also investigated. The expression of ARRB2 was significantly higher in MM patients resistant to proteosome inhibitor (bortezomib) treatment compared to those who responded. Higher ARRB2 expression in the BM of newly diagnosed MM patients was associated with inferior progression-free survival and overall survival. PD-1 expression was downregulated in CD3 T cells isolated from ARRB2 knockout (KO) mice. Furthermore, knockdown of ARRB2 with siRNA reduced PD-1 expression in murine CD3 T cells and PD-L1 expression in murine myeloid-derived suppressor cells. These findings suggest an important role of ARRB2 in MM pathogenesis, potentially mediated via modulation of immune checkpoints in the tumor microenvironment. Our study provides new evidence that ARRB2 may have non-canonical functions independent of GPCRs with relevance to the understanding of MM pathobiology as well as immunotherapy and checkpoint inhibitor escape/resistance more broadly. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Myeloma)
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Review

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21 pages, 1826 KiB  
Review
Selinexor’s Immunomodulatory Impact in Advancing Multiple Myeloma Treatment
by Kereshmeh Tasbihi and Heiko Bruns
Cells 2025, 14(6), 430; https://doi.org/10.3390/cells14060430 - 13 Mar 2025
Viewed by 728
Abstract
Despite the major advancements in the repertoire for multiple myeloma (MM) treatment, this disease remains a chronically progressive plasma cell malignancy. Drug resistance and high relapse rates complicate the extended treatment strategies. However, the tumor microenvironment (TME) in MM is decisive for the [...] Read more.
Despite the major advancements in the repertoire for multiple myeloma (MM) treatment, this disease remains a chronically progressive plasma cell malignancy. Drug resistance and high relapse rates complicate the extended treatment strategies. However, the tumor microenvironment (TME) in MM is decisive for the success of a therapy or relapse. Aiming to improve the outcome of relapsed and refractory MM patients, Selinexor has entered the drug arsenal of myeloma therapy through the implementation of a novel therapeutic approach by selectively inhibiting the nuclear export receptor Exportin-1 (XPO1). Selinexor leads to the inactivation of cancer-related proteins and induces apoptosis by disrupting the nucleocytoplasmic flow in myeloma cells. While this drug is selectively cytotoxic to neoplastic cells, Selinexor’s immunomodulatory impact on the TME is currently being investigated. The aim of this review was to elucidate Selinexor’s capacity to influence the cell interaction network of the TME from an immunological perspective. Deciphering the complex interplay of highly plastic immune cells provides a contribution to the molecular–biological exploration of disease initiation and progression in MM. Unraveling the novel therapeutic targets of the immunological TME and evaluating the advanced immunotherapeutic regimens implementing Selinexor will shape the future directions of immune-oncotherapy in MM. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms and Therapy of Myeloma)
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