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Molecular Mechanisms of Lung Cancer and Mesothelioma

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 December 2022) | Viewed by 31069

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Prof. Rajkumar Savai

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Guest Editor

Molecular Mechanisms in Lung Cancer, Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, D-61231 Bad Nauheim, Germany

Prof. Dr. Michael Thomas

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Guest Editor

Department of Thoracic Oncology, Thoraxklinik at Heidelberg University Hospital, 69126 Heidelberg, Germany
Interests: lung cancer; deep learning; chemotherapy; radiotherapy

Special Issue Information

Dear Colleagues,

Lung cancer research has become an epicentre of cancer research due to its increased morbidity and mortality in recent years. Despite paradigm-shifting therapeutic development, lung cancer remains universally lethal because of its three biggest challenges: late diagnosis, few treatment advances for early-stage cancer, and discrepancy in cancer care worldwide and within countries. Therefore, improving outcomes requires more than just drug research, but additional items such as improved screening strategies, innovations in medicines, and quality in lung cancer management, suggesting lung cancer research needs to be oriented towards a comprehensive understanding of lung cancer's molecular biology.

Another type of lung cancer that begins not in the lung, but in the pleural lining around the lungs and chest is known as Pleural mesothelioma. It is mainly caused by asbestos exposure in the workplace. The incidence of this cancer was rare until the widespread use of asbestos started in the mid-20th century in the construction sector. In Western countries, strict regulation on the use of asbestos led to a reduction in new cases. Still, its long latency and continued use in non-Western countries make pleural mesothelioma a global problem. Low life expectancy following a diagnosis, high mortality rate, and only modest survival improvements even with the best therapeutic approaches suggests that available treatment is reaching a therapeutic plateau. Therefore, an extensive understanding of pleural mesothelioma's molecular biology is a “need of the hour” for therapeutic progress.

The Special Issue "Molecular Biology of Lung Cancer and Mesothelioma" aims to bring together original research and review articles that will illustrate recent advances in the area of molecular biology of lung cancer and mesothelioma.

Prof. Rajkumar Savai
Prof. Michael Thomas
Guest Editors

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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

Lung cancer
Mesothelioma
Tumor microenvironment
Stromal cells
Immune evasion
Extracellular matrix
Metastasis
Genomic and epigenomic molecular alterations
Mechanistic insights
Therapeutics approaches
Drug resistance
Translational research
Novel tools for diagnostics
Diagnostic and prognostic markers

Published Papers (12 papers)

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Research

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13 pages, 488 KiB

Open AccessArticle

ARDS after Pneumonectomy: How to Prevent It? Development of a Nomogram to Predict the Risk of ARDS after Pneumonectomy for Lung Cancer

by Antonio Mazzella, Shehab Mohamed, Patrick Maisonneuve, Alessandro Borri, Monica Casiraghi, Luca Bertolaccini, Francesco Petrella, Giorgio Lo Iacono and Lorenzo Spaggiari

Cancers 2022, 14(24), 6048; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14246048 - 08 Dec 2022

Cited by 1 | Viewed by 1203

Abstract

(1) Background: The cause of ARDS after pneumonectomy is still unclear, and the study of risk factors is a subject of debate. (2) Methods: We reviewed a large panel of pre-, peri- and postoperative data of 211 patients who underwent pneumonectomy during the period 2014–2021. Univariable and multivariable logistic regression was used to quantify the association between preoperative parameters and the risk of developing ARDS, in addition to odds ratios and their respective 95% confidence intervals. A backward stepwise selection approach was used to limit the number of variables in the final multivariable model to significant independent predictors of ARDS. A nomogram was constructed based on the results of the final multivariable model, making it possible to estimate the probability of developing ARDS. Statistical significance was defined by a two-tailed p-value < 0.05. (3) Results: Out of 211 patients (13.3%), 28 developed ARDS. In the univariate analysis, increasing age, Charlson Comorbidity Index and ASA scores, DLCO < 75% predicted, preoperative C-reactive protein (CRP), lung perfusion and duration of surgery were associated with ARDS; a significant increase in ARDS was also observed with decreasing VO2max level. Multivariable analysis confirmed the role of ASA score, DLCO < 75% predicted, preoperative C-reactive protein and lung perfusion. Using the nomogram, we classified patients into four classes with rates of ARDS ranking from 2.0% to 34.0%. (4) Conclusions: Classification in four classes of growing risk allows a correct preoperative stratification of these patients in order to quantify the postoperative risk of ARDS and facilitate their global management. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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20 pages, 7508 KiB

Open AccessArticle

Lung Adenocarcinoma Cell Sensitivity to Chemotherapies: A Spotlight on Lipid Droplets and SREBF1 Gene

by Anna Ricarda Gründing, Marc A. Schneider, Sarah Richtmann, Mark Kriegsmann, Hauke Winter, Beatriz Martinez-Delgado, Sarai Varona, Bin Liu, David S. DeLuca, Julia Held, Sabine Wrenger, Thomas Muley, Michael Meister, Tobias Welte and Sabina Janciauskiene

Cancers 2022, 14(18), 4454; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14184454 - 14 Sep 2022

Viewed by 2116

Abstract

To explore the relationship between cancer cell SREBF1 expression, lipid droplets (LDs) formation, and the sensitivity to chemotherapies, we cultured lung adenocarcinoma cells H1299 (with LD) and H1563 (without LD) in a serum-free basal medium (BM) or neutrophil degranulation products containing medium (NDM), and tested cell responses to cisplatin and etoposide. By using the DESeq2 Bioconductor package, we detected 674 differentially expressed genes (DEGs) associated with NDM/BM differences between two cell lines, many of these genes were associated with the regulation of sterol and cholesterol biosynthesis processes. Specifically, SREBF1 markedly declined in both cell lines cultured in NDM or when treated with chemotherapeutics. Despite the latter, H1563 exhibited LD formation and resistance to etoposide, but not to cisplatin. Although H1299 cells preserved LDs, these cells were similarly sensitive to both drugs. In a cohort of 292 patients with non-small-cell lung cancer, a lower SREBF1 expression in tumors than in adjacent nontumor tissue correlated with overall better survival, specifically in patients with adenocarcinoma at stage I. Our findings imply that a direct correlation between SREBF1 and LD accumulation can be lost due to the changes in cancer cell environment and/or chemotherapy. The role of LDs in lung cancer development and response to therapies remains to be examined in more detail. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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15 pages, 2357 KiB

Open AccessArticle

EGFR Inhibition Strongly Modulates the Tumour Immune Microenvironment in EGFR-Driven Non-Small-Cell Lung Cancer

by Carolin Selenz, Anik Compes, Marieke Nill, Sven Borchmann, Margarete Odenthal, Alexandra Florin, Johannes Brägelmann, Reinhard Büttner, Lydia Meder and Roland T. Ullrich

Cancers 2022, 14(16), 3943; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14163943 - 16 Aug 2022

Cited by 9 | Viewed by 2182

Abstract

EGFR-driven non-small-cell lung cancer (NSCLC) patients are currently treated with TKIs targeting EGFR, such as erlotinib or osimertinib. Despite a promising initial response to TKI treatment, most patients gain resistance to oncogene-targeted therapy, and tumours progress. With the development of inhibitors against immune checkpoints, such as PD-1, that mediate an immunosuppressive microenvironment, immunotherapy approaches attempt to restore a proinflammatory immune response in tumours. However, this strategy has shown only limited benefits in EGFR-driven NSCLC. Approaches combining EGFR inhibition with immunotherapy to stimulate the immune response and overcome resistance to therapy have been limited due to insufficient understanding about the effect of EGFR-targeting treatment on the immune cells in the TME. Here, we investigate the impact of EGFR inhibition by erlotinib on the TME and its effect on the antitumour response of the immune cell infiltrate. For this purpose, we used a transgenic conditional mouse model to study the immunological profile in EGFR-driven NSCLC tumours. We found that EGFR inhibition mediated a higher infiltration of immune cells and increased local proliferation of T-cells in the tumours. Moreover, inhibiting EGFR signalling led to increased activation of immune cells in the TME. Most strikingly, combined simultaneous blockade of EGFR and anti-PD-1 (aPD-1) enhanced tumour treatment response in a transgenic mouse model of EGFR-driven NSCLC. Thus, our findings show that EGFR inhibition promotes an active and proinflammatory immune cell infiltrate in the TME while improving response to immune checkpoint inhibitors in EGFR-driven NSCLC. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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15 pages, 2321 KiB

Open AccessArticle

Sarcopenia as a Predictor of Short- and Long-Term Outcomes in Patients Surgically Treated for Malignant Pleural Mesothelioma

by Eleonora Faccioli, Stefano Terzi, Chiara Giraudo, Andrea Zuin, Antonella Modugno, Francesco Labella, Giovanni Zambello, Giulia Lorenzoni, Marco Schiavon, Dario Gregori, Giulia Pasello, Fiorella Calabrese, Andrea Dell’Amore and Federico Rea

Cancers 2022, 14(15), 3699; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14153699 - 29 Jul 2022

Cited by 1 | Viewed by 1483

Abstract

Surgery for malignant pleural mesothelioma (MPM) should be reserved only for patients who have a good performance status. Sarcopenia, a well-known predictor of poor outcomes after surgery, is still underinvestigated in MPM. The aim of this study is to evaluate the role of sarcopenia as a predictor of short-and long-term outcomes in patients surgically treated for MPM. In our analysis, we included patients treated with a cytoreductive intent in a multimodality setting, with both pre- and post-operative CT scans without contrast available. We excluded those in whom a complete macroscopic resection was not achieved. Overall, 86 patients were enrolled. Sarcopenia was assessed by measuring the mean muscular density of the bilateral paravertebral muscles (T12 level) on pre-and post-operative CTs; a threshold value of 30 Hounsfield Units (HU) was identified. Sarcopenia was found pre-operatively in 57 (66%) patients and post-operatively in 61 (74%). Post-operative sarcopenic patients had a lower 3-year overall survival (OS) than those who were non-sarcopenic (34.9% vs. 57.6% p = 0.03). Pre-operative sarcopenia was significantly associated with a higher frequency of post-operative complications (65% vs. 41%, p = 0.04). The evaluation of sarcopenia, through a non-invasive method, would help to better select patients submitted to surgery for MPM in a multimodality setting. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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16 pages, 2153 KiB

Open AccessArticle

A Real-World Systematic Analysis of Driver Mutations’ Prevalence in Early- and Advanced-Stage NSCLC: Implications for Targeted Therapies in the Adjuvant Setting

by Irene Terrenato, Cristiana Ercolani, Anna Di Benedetto, Enzo Gallo, Elisa Melucci, Beatrice Casini, Francesca Rollo, Aldo Palange, Paolo Visca, Edoardo Pescarmona, Enrico Melis, Filippo Gallina, Andrea Sacconi, Fabiana Letizia Cecere, Lorenza Landi, Federico Cappuzzo, Gennaro Ciliberto and Simonetta Buglioni

Cancers 2022, 14(12), 2971; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14122971 - 16 Jun 2022

Cited by 7 | Viewed by 2620

Abstract

The approval of osimertinib for adjuvant treatment of stage I–II–III EGFR-mutated NSCLC (early stage) represents a paradigm shift, raising the question of whether other genotype-matched therapeutics approved for advanced-stage NSCLC can also provide clinical benefit in the adjuvant setting. However, there is a paucity of real-world data on the prevalence of actionable genomic alterations (GAs) in early-stage NSCLC. We used next-generation sequencing, complemented by immunohistochemistry and fluorescence in situ hybridization, to screen our single-institution cohort of 1961 NSCLC consecutive cases for actionable molecular targets. The prevalence of actionable GAs was comparable in early versus advanced-stage NSCLC, the only exception being KRAS mutations (more frequent in early-stage cases). Consistent with advanced-stage tumors being more aggressive, co-occurrence of TP53 and EGFR GAs as well as copy number gains were less frequent in early-stage tumors. EGFR mutations and high expression of PD-L1 were inversely associated, whereas KRAS mutations and high PD-L1 reactivity showed positive association. Recapitulating advanced-stage tumors, early-stage NSCLC had the highest share of EGFR mutations in lepidic and acinar subtypes. Resected lepidic tumors contained the highest proportion of the KRAS G12C actionable variant. These results, obtained with routine diagnostic technologies in an unselected clinical setting, provide a significant addition of real-world data in early-stage NSCLC. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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11 pages, 830 KiB

Open AccessArticle

Serum and Pleural Soluble Cell Adhesion Molecules in Mesothelioma Patients: A Retrospective Cohort Study

by Sofia Tsagkouli, Ioannis G. Kyriakoulis, Konstantinos G. Kyriakoulis, Eleni Fyta, Alexandros Syrigos, Petros Bakakos, Adrianni Charpidou and Elias Kotteas

Cancers 2022, 14(12), 2825; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14122825 - 08 Jun 2022

Cited by 1 | Viewed by 1919

Abstract

Mesothelioma, a malignant neoplasm of mesothelial cells, has overall poor prognosis. Cell adhesion molecules (CAMs) are proteins that contribute to the immune response. In this study the clinical utility and prognostic significance of serum and pleural fluid soluble CAM (sCAM) levels were assessed in patients with mesothelioma. Mesothelioma patients were retrospectively recruited (2016–2020). Clinical characteristics, serum and pleural sCAM levels (sE-cadherin, sE-selectin, intercellular adhesion molecule 1 (sICAM-1) and vascular cell adhesion molecule 1 (sVCAM-1)) and histopathological characteristics were gathered. A total of 51 healthy controls were also recruited for a secondary cross-sectional analysis. 92 mesothelioma patients were analyzed (mean age 64.5 years, 87% males, performance status 0–2). Patients with increased pleural sE-cadherin had higher risk for disease progression (adjusted HR 1.11 (1.02, 1.20), p = 0.013). Serum and pleural sE-selectin were decreased in patients with high-grade mesothelioma. Patients with increased serum or pleural sE-selectin levels had lower risk for death (adjusted HR 0.88 (0.81, 0.96), p = 0.003; 0.90 (0.82, 0.99), p = 0.039, respectively). Serum sE-cadherin, sE-selectin and sICAM-1 levels were significantly increased in mesothelioma patients compared to healthy controls. Further studies are needed to indicate the clinical utility of serum and pleural sCAMs in mesothelioma patients. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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14 pages, 2941 KiB

Open AccessArticle

Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells

by Hoi-Hin Kwok, Boning Gao, Koon-Ho Chan, Mary Sau-Man Ip, John Dorrance Minna and David Chi-Leung Lam

Cancers 2021, 13(21), 5345; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13215345 - 25 Oct 2021

Cited by 8 | Viewed by 2053

Abstract

Tobacco smoking is the top risk factor for lung cancer development. Nicotine in cigarettes can induce addiction, and its derivatives become potent carcinogens after metabolic activation and activate oncogenic signaling in lung epithelial cells through their expressed nicotinic acetylcholine receptors (nAChRs). However, the effects of smoking on the tumor immune microenvironment are under investigation. In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit α7 (nAChRα7, CHRNA7) would induce PD-L1 expression in lung epithelial cells. The expression levels of nAChRα7 and PD-L1 in eight human bronchial epithelial cell (HBEC) lines were measured after treatment with cigarette smoke extract (CSE) or nicotine derivatives. The results showed that PD-L1 expression levels increased in HBECs after exposure to CSE or nicotine derivatives. This induction of PD-L1 expression could be diminished by treatment with CHRNA7 small-interfering RNA, and the relevant signaling was mediated via STAT3 phosphorylation and NRF2 expression. In summary, this study demonstrated that the well-known nicotine derivative-activated nAChRα7 could induce STAT3/NRF2 pathways and subsequently promote PD-L1 expression in normal lung epithelial cells. This information provides mechanistic insight into cigarette smoke-induced immune evasion in lung epithelial cells. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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14 pages, 3689 KiB

Open AccessArticle

Finite Element Analysis of the Microwave Ablation Method for Enhanced Lung Cancer Treatment

by Marija Radmilović-Radjenović, Martin Sabo, Marta Prnova, Lukaš Šoltes and Branislav Radjenović

Cancers 2021, 13(14), 3500; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13143500 - 13 Jul 2021

Cited by 19 | Viewed by 2988

Abstract

Knowledge of the frequency dependence of the dielectric properties of the lung tissues and temperature profiles are essential characteristics associated with the effective performance of microwave ablation. In microwave ablation, the electromagnetic wave propagates into the biological tissue, resulting in energy absorption and providing the destruction of cancer cells without damaging the healthy tissue. As a consequence of the respiratory movement of the lungs, however, the accurate prediction of the microwave ablation zone has become an exceptionally demanding task. For that purpose, numerical modeling remains a primordial tool for carrying out a parametric study, evaluating the importance of the inherent phenomena, and leading to better optimization of the medical procedure. This paper reports on simulation studies on the effect of the breathing process on power dissipation, temperature distribution, the fraction of damage, and the specific absorption rate during microwave ablation. The simulation results obtained from the relative permittivity and conductivity for inflated and deflated lungs are compared with those obtained regardless of respiration. It is shown that differences in the dielectric properties of inflated and deflated lungs significantly affect the time evolution of the temperature and its maximum value, the time, the fraction of damage, and the specific absorption rate. The fraction of damage determined from the degree of tissue injury reveals that the microwave ablation zone is significantly larger under dynamic physical parameters. At the end of expiration, the ablation lesion area is more concentrated around the tip and slot of the antenna, and the backward heating effect is smaller. The diffuse increase in temperature should reach a certain level to destroy cancer cells without damaging the surrounding tissue. The obtained results can be used as a guideline for determining the optimal conditions to improve the overall success of microwave ablation. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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Review

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20 pages, 1077 KiB

Open AccessReview

Osimertinib Resistance: Molecular Mechanisms and Emerging Treatment Options

by Georgia Gomatou, Nikolaos Syrigos and Elias Kotteas

Cancers 2023, 15(3), 841; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15030841 - 30 Jan 2023

Cited by 14 | Viewed by 5059

Abstract

The development of tyrosine kinase inhibitors (TKIs) targeting the mutant epidermal growth factor receptor (EGFR) protein initiated the success story of targeted therapies in non-small-cell lung cancer (NSCLC). Osimertinib, a third-generation EGFR-TKI, is currently indicated as first-line therapy in patients with NSCLC with sensitizing EGFR mutations, as second-line therapy in patients who present the resistance-associated mutation T790M after treatment with previous EGFR-TKIs, and as adjuvant therapy for patients with early stage resected NSCLC, harboring EGFR mutations. Despite durable responses in patients with advanced NSCLC, resistance to osimertinib, similar to other targeted therapies, inevitably develops. Understanding the mechanisms of resistance, including both EGFR-dependent and -independent molecular pathways, as well as their therapeutic potential, represents an unmet need in thoracic oncology. Interestingly, differential resistance mechanisms develop when osimertinib is administered in a first-line versus second-line setting, indicating the importance of selection pressure and clonal evolution of tumor cells. Standard therapeutic approaches after progression to osimertinib include other targeted therapies, when a targetable genetic alteration is detected, and cytotoxic chemotherapy with or without antiangiogenic and immunotherapeutic agents. Deciphering the when and how to use immunotherapeutic agents in EGFR-positive NSCLC is a current challenge in clinical lung cancer research. Emerging treatment options after progression to osimertinib involve combinations of different therapeutic approaches and novel EGFR-TKI inhibitors. Research should also be focused on the standardization of liquid biopsies in order to facilitate the monitoring of molecular alterations after progression to osimertinib. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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14 pages, 2154 KiB

Open AccessReview

KRAS Pathway Alterations in Malignant Pleural Mesothelioma: An Underestimated Player

by Lilith Trassl and Georgios T. Stathopoulos

Cancers 2022, 14(17), 4303; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14174303 - 02 Sep 2022

Cited by 5 | Viewed by 2041

Abstract

Malignant pleural mesothelioma (MPM) is a rare, incurable cancer of the mesothelial cells lining the lungs and the chest wall that is mainly caused by asbestos inhalation. The molecular mechanisms of mesothelial carcinogenesis are still unclear despite comprehensive studies of the mutational landscape of MPM, and the most frequently mutated genes BAP1, NF2, CDKN2A, TP53, and TSC1 cannot cause MPM in mice in a standalone fashion. Although KRAS pathway alterations were sporadically detected in older studies employing targeted sequencing, they have been largely undetected by next generation sequencing. We recently identified KRAS mutations and copy number alterations in a significant proportion of MPM patients. Here, we review and analyze multiple human datasets and the published literature to show that, in addition to KRAS, multiple other genes of the KRAS pathway are perturbed in a significant proportion of patients with MPM. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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12 pages, 464 KiB

Open AccessReview

Analysis of Molecular Biomarkers in Resected Early-Stage Non-Small Cells Lung Cancer: A Narrative Review

by Filippo Tommaso Gallina, Luca Bertolaccini, Daniele Forcella, Shehab Mohamed, Serena Ceddia, Enrico Melis, Francesca Fusco, Claudia Bardoni, Daniele Marinelli, Simonetta Buglioni, Paolo Visca, Federico Cappuzzo, Lorenzo Spaggiari and Francesco Facciolo

Cancers 2022, 14(8), 1949; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14081949 - 13 Apr 2022

Cited by 3 | Viewed by 1980

Abstract

Next-generation sequencing has become a cornerstone in clinical oncology practice and is recommended for the appropriate use of tailored therapies in NSCLC. While NGS has already been standardised in advanced-stage NSCLC, its use is still uncommon in the early stages. The recent approval of Osimertinib for resected EGFR-mutated NSCLC in an adjuvant setting has launched the hypothesis that other targeted therapies used in metastatic patients can also lead to improved early-stage outcomes of NSCLC. The impact of molecular biomarkers on the prognosis of patients undergoing radical surgery for NSCLC is still unclear. Notably, the heterogeneous populations included in the studies that analysed surgical patients could be the main reason for these results. In this review, we report the most important studies that analysed the impact of principal molecular biomarkers on the survival outcomes of patients who underwent radical surgery for NSCLC. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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21 pages, 387 KiB

Open AccessReview

Current Management and Future Perspective in Pleural Mesothelioma

by Rajiv Shah, Laura V. Klotz and Julia Glade

Cancers 2022, 14(4), 1044; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14041044 - 18 Feb 2022

Cited by 6 | Viewed by 3786

Abstract

Pleural mesothelioma is an aggressive malignancy arising from pleural mesothelial cell lining, predominantly associated with prior exposure to asbestos. The ban on asbestos use has led to its lower incidence in many countries, but globally the disease burden is expected to rise. Therefore, well-planned research is needed to develop more effective, tolerable and affordable drugs. The development of novel treatment has been too slow, with only two regimens of systemic therapy with robust phase 3 data approved formally to date. The treatment scenario for resectable disease remains controversial. However, recent developments in the understanding of disease and clinical trials have been encouraging, and may add better treatment options in the coming years. In this review, we discuss the current treatment options for pleural mesothelioma and shed light on some recent studies and ongoing trials. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Lung Cancer and Mesothelioma)

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