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Cells
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Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma
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Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 January 2020) | Viewed by 24898

Special Issue Editors

Prof. Ramon Garcia Sanz

E-Mail Website
Guest Editor
Hematology Department, Hospital Universitario de Salamanca, Salamanca, Spain
Interests: molecular genetics; multiple myeloma; Hodgkin’s lymphoma; Waldenström macroglobulinemia
Special Issues, Collections and Topics in MDPI journals
Prof. Norma C. Gutiérrez

E-Mail Website
Guest Editor
Hematology Department, Hospital Universitario de Salamanca, Salamanca, Spain
Interests: cytogenetics; multiple myeloma; central nervous system lymphoma; transplant

Special Issue Information

Dear Colleagues,

Multiple Myeloma (MM) is a neoplastic disorder characterized by the accumulation of plasma cells that produce a monoclonal immunoglobulin, accompanied by bone destruction, hypercalcemia, medullar insufficiency or renal impairment. Recent advances in technology, such as the new high-throughput genomic methodologies, gene editing methods, next generation flow and mass cytometry, and novel imaging techniques have generated a huge amount of information about myeloma pathogenesis. Accordingly, many new cellular and molecular insights have emerged in myeloma, which makes a comprehensive review of the current biology of the disease compulsory.

This Special Issue of Cells will focus on the current molecular and cellular mechanisms of multiple myeloma. It will include reviews and original reports focused on cell ontogeny, signaling pathways, microenvironment and genomics of myeloma cells. New diagnostic and monitoring possibilities will also be covered, including blood, bone marrow and skeletal evaluation of the disease, especially for the evaluation of minimal residual disease, the new goal for multiple myeloma therapy. Finally, the evaluation of potential new targets and mechanisms of resistance will also be considered in the issue, providing information towards possible cures for this disease.

We are pleased to present this Special Issue of Cells, with the hope that it will be of value to all interested in myeloma.

Prof. Ramon Garcia Sanz
Prof. Norma C. Gutiérrez
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

  • normal and myelomatous plasma cell ontogeny
  • signaling pathways in myeloma
  • microenvironment in plasma cell dyscrasias
  • genetic abnormalities in multiple myeloma
  • clues for tumor progression: from normal B-cells to plasma cell myeloma
  • blood biopsies in monoclonal gammopathies
  • minimal residual disease in multiple myeloma
  • bone disease in MM
  • new targets in the therapeutics of MM
  • biological background of drug resistance in multiple myeloma

Published Papers (5 papers)

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Research

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15 pages, 2756 KiB  
Article
Distinct Nuclear Organization of Telomeres and Centromeres in Monoclonal Gammopathy of Undetermined Significance and Multiple Myeloma
by Pak Lok Ivan Yu, Rachel R. Wang, Grace Johnston, Yaqiong Wang, Pille Tammur, Anu Tamm, Mari Punab, Aline Rangel-Pozzo and Sabine Mai
Cells 2019, 8(7), 723; https://doi.org/10.3390/cells8070723 - 15 Jul 2019
Cited by 2 | Viewed by 2959
Abstract
Both multiple myeloma (MM) and its precursor state of monoclonal gammopathy of undetermined significance (MGUS) are characterized by an infiltration of plasma cells into the bone marrow, but the mechanisms underlying the disease progression remain poorly understood. Previous research has indicated that 3D [...] Read more.
Both multiple myeloma (MM) and its precursor state of monoclonal gammopathy of undetermined significance (MGUS) are characterized by an infiltration of plasma cells into the bone marrow, but the mechanisms underlying the disease progression remain poorly understood. Previous research has indicated that 3D nuclear telomeric and centromeric organization may represent important structural indicators for numerous malignancies. Here we corroborate with previously noted differences in the 3D telomeric architecture and report that modifications in the nuclear distribution of centromeres may serve as a novel structural marker with potential to distinguish MM from MGUS. Our findings improve the current characterization of the two disease stages, providing two structural indicators that may become altered in the progression of MGUS to MM. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma)
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16 pages, 4514 KiB  
Article
Systemic Dysfunction of Osteoblast Differentiation in Adipose-Derived Stem Cells from Patients with Multiple Myeloma
by Véronique Béréziat, Christelle Mazurier, Martine Auclair, Nathalie Ferrand, Séverine Jolly, Tiffany Marie, Ladan Kobari, Indira Toillon, François Delhommeau, Bruno Fève, Annette K. Larsen, Michèle Sabbah and Laurent Garderet
Cells 2019, 8(5), 441; https://doi.org/10.3390/cells8050441 - 10 May 2019
Cited by 12 | Viewed by 3687
Abstract
Multiple myeloma is characterized by bone lesions linked to increased osteoclast and decreased osteoblast activities. In particular, the osteoblast differentiation of bone marrow-derived stem cells (MSC) is impaired. Among the potential therapeutic tools for counteracting bone lesions, adipose-derived stem cells (ASC) could represent [...] Read more.
Multiple myeloma is characterized by bone lesions linked to increased osteoclast and decreased osteoblast activities. In particular, the osteoblast differentiation of bone marrow-derived stem cells (MSC) is impaired. Among the potential therapeutic tools for counteracting bone lesions, adipose-derived stem cells (ASC) could represent an appealing source for regenerative medicine due to their similar characteristics with MSC. Our study is among the first giving detailed insights into the osteoblastogenic capacities of ASC isolated by fat aspiration from myeloma patients (MM-ASC) compared to healthy subjects (HD-ASC). We showed that MM-ASC and HD-ASC exhibited comparable morphology, proliferative capacity, and immunophenotype. Unexpectedly, although normal in adipocyte differentiation, MM-ASC present a defective osteoblast differentiation, as indicated by less calcium deposition, decreased alkaline phosphatase activity, and downregulation of RUNX2 and osteocalcin. Furthermore, these ASC-derived osteoblasts displayed enhanced senescence, as shown by an increased β-galactosidase activity and cell cycle inhibitors expression (p16INK4A, p21WAF1/CIP1.), associated with a markedly increased expression of DKK1, a major inhibitor of osteoblastogenesis in multiple myeloma. Interestingly, inhibition of DKK1 attenuated senescence and rescued osteoblast differentiation, highlighting its key role. Our findings show, for the first time, that multiple myeloma is a systemic disease and suggest that ASC from patients would be unsuitable for tissue engineering designed to treat myeloma-associated bone disease. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma)
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Review

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38 pages, 1060 KiB  
Review
Immunotherapy in Multiple Myeloma
by Cinnie Yentia Soekojo, Melissa Ooi, Sanjay de Mel and Wee Joo Chng
Cells 2020, 9(3), 601; https://doi.org/10.3390/cells9030601 - 03 Mar 2020
Cited by 28 | Viewed by 5381
Abstract
Multiple myeloma is a complex disease and immune dysfunction has been known to play an important role in the disease pathogenesis, progression, and drug resistance. Recent efforts in drug development have been focused on immunotherapies to modify the MM disease process. Here, we [...] Read more.
Multiple myeloma is a complex disease and immune dysfunction has been known to play an important role in the disease pathogenesis, progression, and drug resistance. Recent efforts in drug development have been focused on immunotherapies to modify the MM disease process. Here, we summarize the emerging immunotherapies in the MM treatment landscape. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma)
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24 pages, 2615 KiB  
Review
Prognosis, Biology, and Targeting of TP53 Dysregulation in Multiple Myeloma
by Erin Flynt, Kamlesh Bisht, Vinidhra Sridharan, María Ortiz, Fadi Towfic and Anjan Thakurta
Cells 2020, 9(2), 287; https://doi.org/10.3390/cells9020287 - 24 Jan 2020
Cited by 39 | Viewed by 6597
Abstract
Multiple myeloma (MM) is the second most common hematological cancer and is characterized by genetic features including translocations, chromosomal copy number aberrations, and mutations in key oncogene and tumor suppressor genes. Dysregulation of the tumor suppressor TP53 is important in the pathogenesis of [...] Read more.
Multiple myeloma (MM) is the second most common hematological cancer and is characterized by genetic features including translocations, chromosomal copy number aberrations, and mutations in key oncogene and tumor suppressor genes. Dysregulation of the tumor suppressor TP53 is important in the pathogenesis of many cancers, including MM. In newly-diagnosed MM patients, TP53 dysregulation occurs in three subsets: monoallelic deletion as part of deletion of chromosome 17p (del17p) (~8%), monoallelic mutations (~6%), and biallelic inactivation (~4%). Del17p is an established high-risk feature in MM and is included in current disease staging criteria. Biallelic inactivation and mutation have also been reported in MM patients but are not yet included in disease staging criteria for high-risk disease. Emerging clinical and genomics data suggest that the biology of high-risk disease is complex, and so far, traditional drug development efforts to target dysregulated TP53 have not been successful. Here we review the TP53 dysregulation literature in cancer and in MM, including the three segments of TP53 dysregulation observed in MM patients. We propose a reverse translational approach to identify novel targets and disease drivers from TP53 dysregulated patients to address the unmet medical need in this setting. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma)
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18 pages, 974 KiB  
Review
Biological Background of Resistance to Current Standards of Care in Multiple Myeloma
by Pedro Mogollón, Andrea Díaz-Tejedor, Esperanza M. Algarín, Teresa Paíno, Mercedes Garayoa and Enrique M. Ocio
Cells 2019, 8(11), 1432; https://doi.org/10.3390/cells8111432 - 13 Nov 2019
Cited by 24 | Viewed by 5709
Abstract
A high priority problem in multiple myeloma (MM) management is the development of resistance to administered therapies, with most myeloma patients facing successively shorter periods of response and relapse. Herewith, we review the current knowledge on the mechanisms of resistance to the standard [...] Read more.
A high priority problem in multiple myeloma (MM) management is the development of resistance to administered therapies, with most myeloma patients facing successively shorter periods of response and relapse. Herewith, we review the current knowledge on the mechanisms of resistance to the standard backbones in MM treatment: proteasome inhibitors (PIs), immunomodulatory agents (IMiDs), and monoclonal antibodies (mAbs). In some cases, strategies to overcome resistance have been discerned, and an effort should be made to evaluate whether resensitization to these agents is feasible in the clinical setting. Additionally, at a time in which we are moving towards precision medicine in MM, it is equally important to identify reliable and accurate biomarkers of sensitivity/refractoriness to these main therapeutic agents with the goal of having more efficacious treatments and, if possible, prevent the development of relapse. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Multiple Myeloma)
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