Comparative proteomic analysis of malignant pleural mesothelioma: Focusing on the biphasic subtype

Our plain-English summary of Comparative proteomic analysis of malignant pleural mesothelioma: Focusing on the biphasic subtype, by L. Giusti, F. Ciregia, A. Bonotti, et al (EuPA Open Proteomics, 2016).

The study

• Authors: L. Giusti, F. Ciregia, A. Bonotti, Y. Da Valle, E. Donadio, C. Boldrini, R. Foddis, G. Giannaccini, M.R. Mazzoni, P.A. Canessa, A. Cristaudo, A. Lucacchini
• Journal: EuPA Open Proteomics
• Published: 2016;10:42-49
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Malignant pleural mesothelioma (MPM) is a rare cancer originated from pleural mesothelial cells. MPM has been associated with long-term exposure to asbestos. In this work we performed a comparative proteomic analysis of biphasic pleural mesothelioma (B-PM). Tissue biopsies were obtained from 61 patients who were subjected to a diagnostic thoracoscopy. 2D/MS based approach was used for proteomic analysis. The 22 proteins found differentially expressed in B-PM, with respect to benign, were analyzed by Ingenuity Pathways Analysis and compared with those obtained for epitheliod pleural mesothelioma (E-PM). A different activation of transcription factors, proteins and cytokines were observed between two subtypes.

In plain English

This laboratory study compared the proteins in pleural tissue biopsies from 61 patients who had a diagnostic thoracoscopy before any treatment. On microscopic examination, 10 samples were biphasic pleural mesothelioma, 23 were epithelioid pleural mesothelioma, 14 were benign (pleural inflammation or hyperplasia) and 14 were lung carcinoma. The patient table recorded asbestos exposure in 6 of the 10 biphasic and 16 of the 23 epithelioid patients. Using two-dimensional gel electrophoresis and mass spectrometry, the authors found 26 protein spots, representing 22 proteins, that differed at least twofold between biphasic mesothelioma and benign tissue. Western blot tests on four of these proteins confirmed a significant increase in biphasic compared with epithelioid mesothelioma only for serum amyloid A1 (p = 0.033) and gamma-enolase (p = 0.042). Computer pathway analysis predicted that Nrf2, IL-6 and TP53 were activated in biphasic mesothelioma but turned off in epithelioid mesothelioma. The authors concluded that the two subtypes show both similarity and divergence. They suggested this could come from different responses of cells to the same harmful agent, asbestos.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory proteomic comparison of human tissue biopsies: two-dimensional gel electrophoresis with mass spectrometry, western blot validation, and computer pathway analysis (Ingenuity Pathway Analysis)
• Who was studied: Tissue biopsies from 61 patients enrolled at diagnosis, before any treatment, who underwent diagnostic thoracoscopy. The samples were 23 epithelioid pleural mesothelioma, 10 biphasic pleural mesothelioma, 14 benign (7 pleural inflammation, 7 hyperplasia) and 14 lung carcinoma. The article does not state where or when patients were enrolled.
• Exposure: The study compared tissue types, not asbestos exposures. Table 1 lists asbestos exposure as present in 16 (70%) of the 23 epithelioid mesothelioma patients, 6 (60%) of the 10 biphasic mesothelioma patients, 5 (36%) of the 14 benign controls and 7 (50%) of the 14 lung carcinoma controls. Fiber types, jobs and doses are not described.
• Main results:
  • In biphasic mesothelioma compared with benign samples, 26 protein spots showed at least a twofold change in expression. These corresponded to 22 different proteins.
  • In western blot validation of four proteins (SAA1, S100A11, gamma-enolase, CLIC3), only serum amyloid A1 (p-value = 0.033) and gamma-enolase (p-value = 0.042) showed a confirmed significant increase in biphasic compared with epithelioid mesothelioma.
  • For all four tested proteins, biphasic mesothelioma differed significantly (p < 0.05) from both the benign samples and the lung carcinoma samples.
  • Pathway analysis predicted that Nrf2, IL-6 and TP53 were activated in biphasic mesothelioma but turned off in epithelioid mesothelioma.
  • For biphasic mesothelioma compared with benign samples, pathway analysis predicted decreased activation of reactive oxygen species synthesis, respiratory system tumor and cell death.
• The authors' conclusion: The authors concluded that their results confirm similarity and suggest divergence between the two mesothelioma subtypes. They proposed that this could arise from different cellular responses to the same harmful agent, asbestos, through different activation or inhibition of transcription factors.

Topics

Medical terms in this study, explained in our Lexicon: Pleural Mesothelioma, Biphasic Mesothelioma, Mesothelial Cells, Thoracoscopy, Cytokine.

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