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Mesothelioma Environmental Risk Factors and Epidemiological and Biological Insights

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

Deadline for manuscript submissions: 10 August 2026 | Viewed by 677

Special Issue Editor


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Guest Editor
Pathology, Flinders Health and Medical Research Institute, Flinders University, Bedford Park, SA 5042, Australia
Interests: mesothelioma; lung cancer; asbestos; mesothelial proliferations

Special Issue Information

Dear Colleagues,

Mesothelioma is a malignant tumor of serosal membranes with protean morphology and complex biology that has long been regarded as a signal tumor for exposure to asbestos. It typically has a poor prognosis, and treatment options remain limited. Owing to a long latency between asbestos exposure and tumor development, case numbers worldwide are expected to remain high for years to come, despite bans on asbestos in many countries. The role of genetic disease predisposition continues to be explored. Personalized and targeted therapy for mesothelioma is in its infancy. Molecular characterization of mesothelial lesions is leading to improved tumor classification, and as our molecular understanding of mesothelial lesions deepens, therapeutic options expand. This Special Issue will explore the global burden of disease, along with factors impacting disease development and all basic and clinical aspects of therapy that advance our understanding, diagnosis and treatment of mesothelial lesions. 

Dr. Sonja Klebe
Guest Editor

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Keywords

  • mesothelioma
  • asbestos
  • mesothelial proliferation
  • therapy
  • marker

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Published Papers (1 paper)

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Research

19 pages, 2315 KB  
Article
A High-Fidelity Patient-Derived Organoid Platform Recapitulates the Dynamic Metabolic Landscape of Cisplatin Tolerance in Mesothelioma
by Zivile Useckaite, Ashleigh J. Hocking, Lauren A. Mortimer, John Salamon, Simon Lee, Yazad Irani, Lucy Franzon, Arya L. Arul, Sarita Prabhakaran and Sonja Klebe
Cancers 2026, 18(10), 1500; https://doi.org/10.3390/cancers18101500 - 7 May 2026
Viewed by 475
Abstract
Background: Pleural mesothelioma (PM) is characterised by often rapid therapeutic failure and chemotherapy resistance. While terminal resistance is well studied, the initial transition into a drug-tolerant phenotype remains poorly understood. Methods: We established patient-derived organoids (PDOs) from malignant pleural effusions to [...] Read more.
Background: Pleural mesothelioma (PM) is characterised by often rapid therapeutic failure and chemotherapy resistance. While terminal resistance is well studied, the initial transition into a drug-tolerant phenotype remains poorly understood. Methods: We established patient-derived organoids (PDOs) from malignant pleural effusions to model this transition. Cisplatin-tolerant lines were generated via repeated incremental exposure to cisplatin and compared to time-matched treatment-naive controls using RNA sequencing and Seahorse XFe96 metabolic flux analysis. Results: Integrated profiling suggested that the route to tolerance may be influenced by the underlying mutational profile. In this cohort, all BAP1-retained models (including those with KRAS mutations or MTAP loss) adopted an elevated basal metabolic hybrid phenotype, significantly upregulating baseline oxidative phosphorylation and glycolysis to fuel survival mechanisms. Conversely, BAP1-deficient models entered a hypometabolic state of dormancy, characterised by baseline bioenergetic suppression and reduced Ki-67 proliferation. Transcriptomic analysis identified a vesicular transport signature (SYNGR3, VPS52, PROM2) in plastic models, suggesting altered membrane trafficking as a potential survival strategy. Conclusions: Our findings demonstrate that mesothelioma therapeutic escape is not a uniform process. Identifying these patient-specific metabolic and transcriptomic trajectories via 3D PDOs provides a hypothesis-generating framework to explore potential avenues for future personalised therapy. Full article
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