Beyond Stanton and Pott hypothesis; carbon nanotubes-induced malignant mesothelioma as a disease of gene loss

Our plain-English summary of Beyond Stanton and Pott hypothesis; carbon nanotubes-induced malignant mesothelioma as a disease of gene loss, by G.J. Yoshida (Journal of Occupational Health, 2019).

The study

• Author: G.J. Yoshida
• Journal: Journal of Occupational Health
• Published: 2019;61(2):203-205
• Type of article: Letter
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

In plain English

This is a letter to the editor, not an original study, and it reports no new data. The author wrote in response to two review articles in the same journal about whether carbon nanotubes (CNTs) can cause cancer in the same way as asbestos. Drawing on those reviews and other published research, the letter described reports that multi-walled CNTs caused peritoneal mesotheliomas in p53 heterozygous mice, and that single-walled CNTs and carbon nanofibers caused DNA double-strand breaks. The author wrote that malignant mesothelioma is considered a "disease of gene loss." The letter cited research linking loss or silencing of the tumor suppressor gene CDKN2A to mesothelioma after exposure to amosite asbestos or long CNTs. It also described a published report that multi-walled CNTs directly pierce the membranes of mesothelial cells, whereas cells enclose asbestos fibers in membranes. The author suggested that mesothelioma's long latency, with decades of chronic inflammation and oxidative DNA damage, may point to a multifactorial mechanism involving epigenetic changes and loss of tumor suppressor genes.

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: Letter to the editor commenting on two review articles; no original research
• Who was studied: No people or animals were studied by the author; the letter discusses previously published animal and laboratory research
• Exposure: Carbon nanotubes (multi-walled and single-walled) and carbon nanofibers, compared with asbestos, including amosite
• Main results:
  • Reported from another publication, not found by this letter: exposure to multi-walled CNTs caused peritoneal mesotheliomas in p53 heterozygous mice
  • Reported from another publication: single-walled CNTs and carbon nanofibers induced DNA double-strand breaks
  • The author described malignant mesothelioma as considered a 'disease of gene loss' rather than one driven by driver mutations, citing another study
  • Reported from another publication: loss of p19 and silencing of p16 (CDKN2A) were associated with mesothelioma progression after exposure to amosite asbestos or long CNTs
  • Reported from another publication: multi-walled CNTs directly pierce mesothelial cell and nuclear membranes, whereas mesothelial cells take in asbestos fibers inside membrane structures
• The authors' conclusion: The author suggested that the long latency of malignant mesothelioma, with decades of chronic inflammation and oxidative DNA damage, may point to a multifactorial disease mechanism including epigenetic changes and loss of tumor suppressor genes such as p16 and p19

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Malignant Mesothelioma.

Related studies

• Long-Fiber Carbon Nanotubes Replicate Asbestos-Induced Mesothelioma with Disruption of the Tumor Suppressor Gene Cdkn2a (Ink4a/Arf) — T. Chernova, F.A. Murphy, et al. (2017)
• Asbestos, carbon nanotubes and the pleural mesothelium: a review of the hypothesis regarding the role of long fibre retention in the parietal pleura, inflammation and mesothelioma — K. Donaldson, F.A. Murphy, et al. (2010)
• Inflammation in the pleural cavity following injection of multi-walled carbon nanotubes is dependent on their characteristics and the presence of IL-1 genes — Y.J. Arnoldussen, V. Skaug, et al. (2018)
• Epithelial-mesenchymal transition involved in pulmonary fibrosis induced by multi-walled carbon nanotubes via TGF-beta/Smad signaling pathway — T. Chen, H. Nie, et al. (2014)
• A single intratracheal instillation of single-walled carbon nanotubes induced early lung fibrosis and subchronic tissue damage in mice — E.J. Park, J. Roh, et al. (2011)
• Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study — B.N. Snyder-Talkington, C. Dong, et al. (2016)

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