Pathogenesis and Treatment Strategies in Multiple Myeloma: From Basic Research to Real Life

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 924

Special Issue Editor


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Guest Editor
Department of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima 770-8503, Japan
Interests: myeloma bone disease; infectious disease in myeloma; proteasome inhibitor; IMiDs; anti-CD38 antibody; venetoclax; immunotherapy

Special Issue Information

Dear Colleagues,

This Special Issue aims to bridge the gap between basic research and clinical practice by providing insights into the underlying mechanisms of multiple myeloma and exploring novel therapeutic approaches. We welcome original articles and comprehensive reviews that dig into various aspects of multiple myeloma, including its molecular pathogenesis, genetic abnormalities, and immune dysregulation with related infectious complications. We also highlight the advancements in diagnostic techniques, prognostic markers, and risk stratification, which play a crucial role in tailoring patients’ personalized treatment plans. Additionally, we discuss the latest developments in targeted therapies, immunotherapies, and combination treatment regimens, shedding light on their efficacy and potential side effects. Furthermore, this Special Issue emphasizes the importance of translational research and the integration of basic science with clinical practice.

Dr. Shingen Nakamura
Guest Editor

Manuscript Submission Information

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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. Cancers 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 2900 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

  • myeloma bone disease
  • denosumab
  • bisphosphonate
  • infectious complication
  • proteasome inhibitor
  • IMiDs
  • anti-CD38 antibody
  • venetoclax
  • immunotherapy

Published Papers (1 paper)

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Review

16 pages, 1676 KiB  
Review
Epigenetic Alterations as Vital Aspects of Bortezomib Molecular Action
by Piotr Kulig, Karolina Łuczkowska, Estera Bakinowska, Bartłomiej Baumert and Bogusław Machaliński
Cancers 2024, 16(1), 84; https://doi.org/10.3390/cancers16010084 - 23 Dec 2023
Viewed by 752
Abstract
Bortezomib (BTZ) is widely implemented in the treatment of multiple myeloma (MM). Its main mechanism of action is very well established. BTZ selectively and reversibly inhibits the 26S proteasome. More precisely, it interacts with the chymotryptic site of the 20S proteasome and therefore [...] Read more.
Bortezomib (BTZ) is widely implemented in the treatment of multiple myeloma (MM). Its main mechanism of action is very well established. BTZ selectively and reversibly inhibits the 26S proteasome. More precisely, it interacts with the chymotryptic site of the 20S proteasome and therefore inhibits the degradation of proteins. This results in the intracellular accumulation of misfolded or otherwise defective proteins leading to growth inhibition and apoptosis. As well as interfering with the ubiquitin–proteasome complex, BTZ elicits various epigenetic alterations which contribute to its cytotoxic effects as well as to the development of BTZ resistance. In this review, we summarized the epigenetic alterations elicited by BTZ. We focused on modifications contributing to the mechanism of action, those mediating drug-resistance development, and epigenetic changes promoting the occurrence of peripheral neuropathy. In addition, there are therapeutic strategies which are specifically designed to target epigenetic changes. Herein, we also reviewed epigenetic agents which might enhance BTZ-related cytotoxicity or restore the sensitivity to BTZ of resistant clones. Finally, we highlighted putative future perspectives regarding the role of targeting epigenetic changes in patients exposed to BTZ. Full article
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