Biologic, cytogenetic, and molecular factors in mesothelial proliferations

Our plain-English summary of Biologic, cytogenetic, and molecular factors in mesothelial proliferations, by J. Hicks (Ultrastructural Pathology, 2006).

The study

• Author: J. Hicks
• Journal: Ultrastructural Pathology
• Published: 2006;30(1):19-30
• Type of article: Review
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Although mesothelioma cases may have peaked in the 1990s in developed countries, it is expected that there will be over 70,000 cases diagnosed in the United States over the next 5 decades. With the industrial expansion in Southeast Asia and China and the continued use of asbestos, an epidemic of mesothelioma cases is anticipated over the next several decades. A considerable amount has been learned about the cytogenetic and molecular genetics of mesotheliomas. However, in-depth studies are needed to further define specific factors that may provide for early diagnosis, surgical treatment, oncologic management, and gene therapy. Serologic markers for surveillance of those with asbestos exposure and at risk for mesothelioma are needed. Targeted therapy using molecular markers and gene therapy may provide a means to reverse mesothelial proliferations or stabilize tumor growth and allow for surgical resection. The future holds great promise in identifying mesothelioma gene expression profiles (genomics, gene microarrays) and proteins (proteomics) that may produce the key to dealing with this dismal and devastating neoplasm.

In plain English

This article was a narrative review by an author from the Department of Pathology at Texas Children's Hospital and Baylor College of Medicine. It reported no new study of its own. It summarized published research on the biology, chromosome changes and gene changes in mesothelioma. Drawing on cited studies, the author wrote that 80% of mesotheliomas are associated with asbestos exposure, that less than 5% of people exposed to asbestos develop mesothelioma, and that the majority of mesotheliomas occur with amphibole fiber exposure. The review stated that standard chromosome analysis (karyotyping) had not found a change specific enough to diagnose mesothelioma. It described a virus, SV40, reported in about 50% of mesotheliomas. It also described animal studies in which asbestos combined with SV40 led to more rapid mesothelioma development. It summarized a cited report in which 7 of 40 healthy asbestos-exposed people had raised blood levels of a protein called mesothelin, and 3 of those 7 later developed mesothelioma. The author concluded that more in-depth studies are needed, and that blood markers are needed to monitor asbestos-exposed people at risk for mesothelioma.

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: Narrative review of published literature (no original data or stated methods)
• Who was studied: No study population of its own. The review compiled findings from 47 cited references on mesothelioma biology, cytogenetics, molecular genetics, SV40 and prognostic markers.
• Exposure: Asbestos in general. The article names 'chrysolite' and amphibole fibers (crocidolite, spelled 'crocridolite' in the article, amosite, tremolite). It also discusses erionite in Turkey and SV40 virus infection.
• Main results:
  • Citing other work, the review stated that 80% of mesotheliomas are associated with asbestos exposure in the environment or the workplace.
  • Citing other work, the review stated that less than 5% of people exposed to asbestos develop mesothelioma.
  • Citing other work, the review stated that most mesotheliomas occur with amphibole fiber exposure.
  • Citing other work, the review gave an estimate of over 70,000 mesothelioma cases in U.S. males between 2003 and 2054.
  • The review stated that karyotyping has not provided chromosome changes specific enough for diagnosis.
  • Citing other work, the review reported SV40 large tumor antigen in about 50% of mesotheliomas.
  • Citing other work, the review reported that in animal models, asbestos combined with SV40 led to faster mesothelioma development.
  • In a cited study of serum mesothelin, 7 of 40 healthy asbestos-exposed individuals with no evidence of tumor had elevated serum mesothelin. Three of these 7 developed mesothelioma 15 to 69 months later. The review described the test as 84% sensitive and 100% specific.
  • In a cited gene-expression ratio study, a test set of 29 mesothelioma patients was checked. Median survival was 35 months for the group the model predicted to have a good outcome, compared with 7 months for the group predicted to have a poor outcome.
• The authors' conclusion: The author concluded that more in-depth studies are needed to define factors for early diagnosis, surgical treatment, oncologic management and gene therapy. The author also stated that serologic (blood) markers are needed for surveillance of asbestos-exposed people at risk for mesothelioma.

Topics

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

Medical terms in this study, explained in our Lexicon: Mesothelioma, Asbestos Exposure, Targeted Therapy, Surgical Resection, Neoplasm.

Related studies

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• BAP1 (BRCA1-associated protein 1) is a highly specific marker for differentiating mesothelioma from reactive mesothelial proliferations — M. Cigognetti, S. Lonardi, et al. (2015)
• Oncofetal protein IMP3, a new diagnostic biomarker to distinguish malignant mesothelioma from reactive mesothelial proliferation — M. Shi, A.E. Fraire, et al. (2011)
• Differential diagnosis of reactive mesothelial cells and malignant mesothelioma cells using the cell proliferation markers minichromosome maintenance protein 7, geminin, topoisomerase II alpha and Ki-67 — F. Kimura, I. Okayasu, et al. (2013)
• Practical utility of insulin-like growth factor II mRNA-binding protein 3, glucose transporter 1, and epithelial membrane antigen for distinguishing malignant mesotheliomas from benign mesothelial proliferations — S. Chang, M.H. Oh, et al. (2014)
• BAP1 immunohistochemistry and p16 FISH to separate benign from malignant mesothelial proliferations — B.S. Sheffield, H.C. Hwang, et al. (2015)

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