bims-mesote Biomed News
on Mesothelioma
Issue of 2026–03–15
six papers selected by
Laura Mannarino, Humanitas Research



  1. Int J Mol Sci. 2026 Feb 25. pii: 2157. [Epub ahead of print]27(5):
      Malignant pleural mesothelioma (MPM) is a rare and aggressive tumor associated with asbestos exposure, which represents a current problem. MPM is characterized by a poor prognosis and an unsatisfactory therapeutic approach. Therefore, improving MPM prognosis is the real challenge for research today. Regarding preclinical data, Transforming Growth Factor-β (TGF-β) plays a crucial role in cancer, and its alteration has been associated with tumor progression and invasiveness, in particular through the Epithelial to Mesenchymal Transition (EMT) event. We investigated the role of TGF-β inhibition in proliferation, cell cycle, migration, and invasiveness in human MPM cells. Data obtained clearly highlighted how TGF-β inhibition, through the silencing or treatment of MPM cells with antibody anti-TGF-β (Fresolimumab), significantly reduces cell proliferation (MTT, PCNA) and prevents metastasis, reducing EMT and decreasing the invasiveness and migration of MPM cells. Finally, we also evaluated TGF-β inhibitory effects in 3D MPM cellular models (spheroids), highlighting a significant slowdown in the growth rate of spheroids treated with anti-TGF-β antibody or Fresolimumab, confirming the results previously obtained. Taken as a whole, targeting TGF-β will represent a starting point for future improvements in MPM management. This is particularly important as we foresee a growing increase in MPM in the coming years.
    Keywords:  Transforming Growth Factor-β (TGF-β); epithelial to mesenchymal transition; invasiveness; malignant pleural mesothelioma; tumor proliferation
    DOI:  https://doi.org/10.3390/ijms27052157
  2. Intern Med. 2026 Mar 10.
      
    Keywords:  Pleural mesothelioma; Thoracoscopy
    DOI:  https://doi.org/10.2169/internalmedicine.6505-25
  3. Mol Imaging Biol. 2026 Mar 09.
       BACKGROUND: Malignant pleural mesothelioma (MPM) poses an imaging challenge that requires special attention, especially in patients who have undergone talc pleurodesis. [18F]FDG PET/CT (FDG PET) is a validated imaging modality in oncology that has proven useful for detecting malignant pleural lesions. However, the inflammatory reaction induced by pleurodesis renders its interpretation unreliable. In this study, we assessed in parallel the role of [11C]Methionine PET/CT (MET PET) and FDG PET in MPM patients before and after talc pleurodesis.
    MATERIALS AND METHODS: We prospectively enrolled 30 consecutive patients with clinical suspicion of MPM who were referred to our Institution from September 2014 to February 2016 for talc pleurodesis. The study was approved and registered at ClinicalTrials.gov (NCT02519049). Patients underwent assessment at baseline and after pleurodesis with two consecutive scans: FDG PET (standard imaging) and MET PET (experimental imaging). Semi-quantitative parameters were defined for both scans and statistically compared to pathological findings from video-assisted thoracoscopy (VATS), including SUVmax, SUVmean, metabolic tumor volume (MTV) and total lesion glycolysis for FDG PET or metabolic tumor burden (TLG or MTB = MTV x SUVmean) for MET PET.
    RESULTS: Twenty patients (M:F = 18:2; median age, 72 years) with MPM (18 epithelioid, 2 non-epithelioid) completed all study investigations. All tumors showed increased uptake of both FDG and MET PET. After talc pleurodesis, FDG PET showed a significant increase in mean and median MTV (P = 0.0005 and 0.0003, respectively) and mean and median TLG (P = 0.0172 and 0.0028, respectively). In contrast, MET PET parameters showed significant increases in mean and median SUVmax (P = 0.0208 and 0.0209, respectively) and SUVmean (P = 0.0106 and 0.0109, respectively) compared to baseline. There was a significant negative correlation between SUVmax, MTV and MTB/TLG and the percentage change at the early assessment post-pleurodesis for both MET PET (rho = -0.645, P < 0.01; rho = -0.517, P = 0.013; rho = -0.528, P = 0.011, respectively) and FDG PET (rho = -0.808, P < 0.01; rho = -0.781, P < 0.01; rho = -0.888, P < 0.01, respectively). The percentage change in SUVmax was significantly greater in FDG PET than for MET PET (+ 19% vs + 16%, P = 0.03). Additionally, mean and median MTV were significantly higher on FDG PET than MET PET (mean + 1022.3 vs + 224.2, P = 0.01; median + 157.5 vs + 7.1, P = 0.02).
    CONCLUSIONS: This study confirms the impact of talc pleurodesis on FDG PET, particularly for volumetric parameters (MTV and TLG). MET PET appears less influenced by post-pleurodesis inflammatory reaction than FDG PET, with changes mostly limited to SUVmax and SUVmean. Clinical Trial Number (NCT02519049) at the Clinical Trial Registry ( https://www.
    CLINICALTRIALS: gov/ ).
    Keywords:  FDG; Inflammation; MPM; Mesothelioma; Methionine; PET/CT; Talc pleurodesis
    DOI:  https://doi.org/10.1007/s11307-026-02093-w
  4. Discov Oncol. 2026 Mar 13.
      
    Keywords:  Heterogeneity; Malignant pleural mesothelioma (MPM); Molecular subtypes; Single-cell RNA sequencing; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s12672-026-04725-7
  5. Genet Med. 2026 Mar 04. pii: S1098-3600(26)00868-3. [Epub ahead of print] 102550
       PURPOSE: Mesothelioma, a disease overwhelmingly driven by asbestos exposure, is also associated with germline genetic changes that interact with asbestos to cause cancer. Very little about barriers to genetic counseling and germline sequencing in mesothelioma patients is known.
    METHODS: We collected DNA, demographic data, and asbestos exposure data from 551 patients with mesothelioma at our center. As part of an IRB-approved study, we sequenced 85 genes associated with hereditary cancer syndromes.
    RESULTS: We identified germline pathogenic or likely pathogenic variants via research-based sequencing in 76 patients (19.1%) who were subsequently offered clinical-grade sequencing. Most (73%) patients declined clinical-grade testing, primarily citing concerns regarding discrimination related to employment, insurance, and asbestos-related litigation.
    CONCLUSIONS: Mesothelioma patients with pathogenic/likely pathogenic germline variants are hesitant to pursue clinical-grade genetic testing, primarily because of discrimination concerns. These concerns likely stem from efforts to use genetic information against these patients in both insurance-related issues and asbestos-related litigation. Because asbestos exposure is the primary cause of mesothelioma, greater legal protections are needed for mesothelioma patients. These protections will enable physicians to optimize the care of patients and their family members, who may also be at risk for asbestos-related cancers and other tumors.
    Keywords:  cancer risk; genetic testing; hereditary cancer syndromes; mesothelioma
    DOI:  https://doi.org/10.1016/j.gim.2026.102550
  6. J Thorac Dis. 2026 Feb 28. 18(2): 166
       Background and Objective: Mesothelioma remains lethal, with a growing share linked to non-occupational exposure in community settings. This review synthesizes contemporary epidemiology, mechanisms, exposure sources, diagnosis, treatment and public health strategies.
    Methods: This narrative review was conducted to synthesize heterogeneous evidence addressing environmental and para-occupational asbestos exposure and its relationship to malignant mesothelioma. A structured literature search was performed using PubMed/MEDLINE, Embase, and Web of Science databases for articles published through 2025. Terms related exclusively to occupational exposure were deliberately deprioritized. Studies were eligible for inclusion if they met at least one of the following criteria: (I) epidemiological investigations evaluating non-occupational, environmental, or para-occupational asbestos exposure; (II) mechanistic or toxicological studies elucidating fiber pathogenicity relevant to environmental exposure scenarios; (III) investigations of population clusters associated with naturally occurring or construction-related mineral fibers; (IV) studies assessing environmental remediation, surveillance strategies, or public-health interventions; or (V) clinical investigations reporting data stratified by exposure category. Articles focusing exclusively on occupational exposure without environmental relevance were excluded. Case reports without exposure characterization, editorials without primary data, and studies lacking clear methodological description were also excluded.
    Key Content and Findings: Environmental risk arises from naturally occurring asbestos (NOA), legacy building materials, industrial residues and para-occupational transfer into homes. Case mix is shifting toward women, younger patients and peritoneal presentations in geologic or industrial hotspots. Fiber biopersistence drives chronic inflammation, oxidative injury and mesothelial transformation. Systemic therapy now centers on dual checkpoint blockade as a first-line standard, with chemo-immunotherapy and platinum-pemetrexed backbones, and selective use of bevacizumab. Surgery is reserved for candidates in expert centers, favoring lung-sparing pleurectomy and decortication when macroscopic clearance is plausible. Prevention requires total prohibition of new asbestos use, disciplined legacy management, robust enforcement, land-use controls in NOA terrains, and household protections.
    Conclusions: Environmental drivers will sustain mesothelioma burden unless exposure pathways are eliminated and legacy sources are controlled. Clinical gains come from immunotherapy, selective surgery and coordinated supportive care, but prevention and earlier detection carry the greatest impact. A unified agenda that couples exposure science with equitable public health action is essential to bend incidence and improve outcomes.
    Keywords:  Mesothelioma; airborne pollutants; asbestos, risk assessment; carcinogenesis
    DOI:  https://doi.org/10.21037/jtd-2025-aw-2134