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Cancers
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Advances in Malignant Pleural Mesothelioma (MPM)
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Advances in Malignant Pleural Mesothelioma (MPM)

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

Deadline for manuscript submissions: closed (10 September 2023) | Viewed by 4805

Special Issue Editors

Dr. Susana Cedrés

E-Mail Website
Guest Editor
Vall d‘Hebron Institut de Oncologia, Barcelona, Spain
Interests: malignant pleural mesothelioma; lung cancer; immune checkpoint inhibitors; immunotherapy
Dr. Santiago Ponce-Aix

E-Mail Website
Guest Editor
Gustave Roussy Cancer Campus Grand Paris, Paris, France
Interests: malignant pleural mesothelioma; non–small cell lung cancer; immunotherapy

Special Issue Information

Dear Colleagues,

Malignant pleural mesothelioma (MPM) is a rare and aggressive cancer associated with asbestos exposure, and its incidence is increasing globally. The complex biology of MPM is poorly understood, and the largest genomic studies to date have demonstrated that mesothelioma is primarily defined by loss-of-function alterations in tumor-suppressor genes. The few available therapeutic options based on chemotherapy or immunotherapy only modestly increase survival, so novel therapeutic approaches are urgently needed. Although predictive biomarkers for systemic therapy are not currently used in clinical practice, insights into the immune microenvironment and genomic landscape of mesothelioma are emerging. Researchers have made important breakthroughs in understanding the biology of MPM, and promising clinical trials may provide better treatment options in the coming years. This Special Issue will describe new developments in the field of biology with genomics and highlight the most relevant data from clinical trials regarding recent treatment strategies for MPM, with a particular focus on immunotherapeutic (e.g., the engineering of T cells to express chimeric antigen receptors (CARs), and dendritic cell (DCs) vaccines) and targeted approaches.

For this Special Issue of Cancers, we invite you to submit original research or a comprehensive review of the state of art of MPM research, including, but not limited to:

  • Histological and molecular characteristics;
  • Radiology and tumor response;
  • Surgery;
  • Molecular alterations;
  • The tumor microenvironment;
  • Targeted agents;
  • Cellular therapies;
  • Predictors of response to immunotherapy;
  • Further trials of interest and future perspectives.

We look forward to receiving your contributions. 

Dr. Susana Cedrés
Dr. Santiago Ponce-Aix
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 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. 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

  • malignant mesothelioma
  • asbestos exposure
  • genomics
  • checkpoint inhibitors
  • immunotherapy
  • targeted therapies

Published Papers (3 papers)

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Research

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20 pages, 6500 KiB  
Article
Evening Primrose Extract Modulates TYMS Expression via SP1 Transcription Factor in Malignant Pleural Mesothelioma
by Małgorzata Chmielewska-Kassassir, Katarzyna Sobierajska, Wojciech M. Ciszewski, Jakub Kryczka, Andrzej Zieleniak and Lucyna A. Wozniak
Cancers 2023, 15(20), 5003; https://doi.org/10.3390/cancers15205003 - 16 Oct 2023
Cited by 1 | Viewed by 1287
Abstract
Purpose: To determine the mechanism of EPE in downregulating TYMS in MPM cancer. Methods: The TYMS mRNA expression with epithelial-to-mesenchymal transition biomarkers and nuclear factor SP1 was assessed using the GEO database in a data set of MPM patients (GSE51024). Invasive MPM cell [...] Read more.
Purpose: To determine the mechanism of EPE in downregulating TYMS in MPM cancer. Methods: The TYMS mRNA expression with epithelial-to-mesenchymal transition biomarkers and nuclear factor SP1 was assessed using the GEO database in a data set of MPM patients (GSE51024). Invasive MPM cell lines were in vitro models for the investigation of TYMS expression after EPE treatment. The tyms promoter SP1 binding sequences were determined using Genomatix v 3.4 software Electrophoretic mobility shift and dual-luciferase reporter assays revealed specific SP1 motifs in the interaction of EPE and reference compounds. Chromatin immunoprecipitation and Re-ChIP were used for the co-occupancy study. Results: In MPM patients, a positive correlation of overexpressed TYMS with mesenchymal TWIST1, FN1 and N-cadherin was observed. EPE and its major components, gallic and ellagic acid (GA and EA, respectively), downregulated TYMS in invasive MPM cells by interacting with particular SP1 motifs on the tyms promoter. The luciferase constructs confirmed the occupation of two SP1 regulatory regions critical for the promotion of TYMS expression. Both EPE and reference standards influenced SP1 translocation into the nucleus. Conclusion: EPE components reduced TYMS expression by occupation of SP1 motifs on the tyms promoter and reversed the EMT phenotype of invasive MPM cells. Further in-depth analysis of the molecular docking of polyphenol compounds with SP1 regulatory motifs is required. Full article
(This article belongs to the Special Issue Advances in Malignant Pleural Mesothelioma (MPM))
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11 pages, 7248 KiB  
Article
Deletions of CDKN2A and MTAP Detected by Copy-Number Variation Array Are Associated with Loss of p16 and MTAP Protein in Pleural Mesothelioma
by Bart Vrugt, Michaela B. Kirschner, Mayura Meerang, Kathrin Oehl, Ulrich Wagner, Alex Soltermann, Holger Moch, Isabelle Opitz and Peter J. Wild
Cancers 2023, 15(20), 4978; https://doi.org/10.3390/cancers15204978 - 13 Oct 2023
Cited by 3 | Viewed by 1513
Abstract
CDKN2A deletion is a common alteration in pleural mesothelioma (PM) and frequently associated with co-deletion of MTAP. Since the standard detection method for CDKN2A deletion and FISH analysis is relatively expensive, we here investigated the suitability of inexpensive p16 and MTAP IHC [...] Read more.
CDKN2A deletion is a common alteration in pleural mesothelioma (PM) and frequently associated with co-deletion of MTAP. Since the standard detection method for CDKN2A deletion and FISH analysis is relatively expensive, we here investigated the suitability of inexpensive p16 and MTAP IHC by comparing concordance between IHC and OncoScan CNV arrays on samples from 52 PM patients. Concordance was determined using Cohen’s kappa statistics. Loss of CDKN2A was associated with co-deletion of MTAP in 71% of cases. CDKN2A-MTAP copy-number normal cases were also IHC positive in 93% of cases for p16 and 100% for MTAP, while homozygous deletion of CDKN2A-MTAP was always associated with negative IHC for both proteins. In cases with heterozygous CDKN2A-MTAP loss, IHC expression of p16 and MTAP was negative in 100% and 71%, respectively. MTAP and p16 IHC showed high sensitivity (MTAP 86.5%, p16 100%) and specificity (MTAP 100%, p16 93.3%) for the detection of any gene loss. Loss of MTAP expression occurred exclusively in conjunction with loss of p16 labeling. Both p16 and MTAP IHC showed high concordance with Oncoscan CNV arrays (kappa = 0.952, p < 0.0001, and kappa = 0.787, p < 0.0001 respectively). We recommend combined MTAP and p16 immunohistochemistry to confirm the diagnosis of PM. Full article
(This article belongs to the Special Issue Advances in Malignant Pleural Mesothelioma (MPM))
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Review

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15 pages, 318 KiB  
Review
Clinical Next Generation Sequencing Application in Mesothelioma: Finding a Golden Needle in the Haystack
by Luigi Cerbone, Sara Orecchia, Pietro Bertino, Sara Delfanti, Antonina Maria de Angelis and Federica Grosso
Cancers 2023, 15(24), 5716; https://doi.org/10.3390/cancers15245716 - 6 Dec 2023
Viewed by 1351
Abstract
Mesothelioma comprises a group of rare cancers arising from the mesothelium of the pleura, peritoneum, tunica vaginalis testis and pericardium. Mesothelioma is generally associated with asbestos exposure and has a dismal prognosis, with few therapeutic options. Several next generation sequencing (NGS) experiments have [...] Read more.
Mesothelioma comprises a group of rare cancers arising from the mesothelium of the pleura, peritoneum, tunica vaginalis testis and pericardium. Mesothelioma is generally associated with asbestos exposure and has a dismal prognosis, with few therapeutic options. Several next generation sequencing (NGS) experiments have been performed on mesothelioma arising at different sites. These studies highlight a genomic landscape mainly characterized by a high prevalence (>20%) of genomic aberrations leading to functional losses in oncosuppressor genes such as BAP1, CDKN2A, NF2, SETD2 and TP53. Nevertheless, to date, evidence of the effect of targeting these alterations with specific drugs is lacking. Conversely, 1–2% of mesothelioma might harbor activating mutations in oncogenes with specifically approved drugs. The goal of this review is to summarize NGS applications in mesothelioma and to provide insights into target therapy of mesothelioma guided by NGS. Full article
(This article belongs to the Special Issue Advances in Malignant Pleural Mesothelioma (MPM))
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