Our plain-English summary of Malignant pleural mesothelioma: newer aspects of carcinogenesis, molecular genetics, and prospects for future therapies, by J.S. Donington, D.J. Mew, H.I. Pass (Surgical Oncology, 1995).
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The study
- Authors: J.S. Donington, D.J. Mew, H.I. Pass
- Journal: Surgical Oncology
- Published: 1995;4(4):175-85
- Type of article: Review
- Cited by: 4 articles, as counted by NIH iCite
- Read it: PubMed · Publisher
Abstract
Malignant pleural mesothelioma (MPM) is an asbestos-related disease which, although rare, is having a major social impact, and is, for the majority of cases, an incurable illness. There has been a surge of information regarding data on mesothelial transformation, mesothelioma molecular genetics and somatic gene therapy for this disease. This report summarizes the most recent investigations attempting to characterize the behaviour, on a cellular and molecular level, of MPM, with an emphasis on data from investigations performed at the National Cancer Institute with our collaborators.
In plain English
This article was a review of recent research on how malignant pleural mesothelioma develops at the cellular and molecular level and on possible gene therapies. It emphasised work by the authors' own group at the National Cancer Institute and their collaborators. It described the two families of asbestos fibres, serpentine (chrysotile) and amphiboles. It also discussed free radicals, chromosome changes, tumour suppressor genes, growth factors and an SV-40-like virus. Among findings from the authors' group, the review reported several results. Crocidolite fibres together with interferon-gamma induced nitric oxide production in mouse macrophages. All nine mesothelioma cell lines analysed had abnormal chromosome patterns. Of 52 tumour specimens, 31 (60%) showed p53 expression, but only 2 of 25 specimens had p53 alterations on mutational analysis. Sixty percent of pleural mesotheliomas removed at the NCI/NIH since 1990 contained SV-40-like DNA. The authors concluded that how this cancer arises is not completely understood. They also concluded that any significant improvement in treatment will come from better understanding of the tumour's cellular and molecular biology.
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 recent laboratory and molecular research on malignant pleural mesothelioma, emphasising the authors' own group's work
- Who was studied: Published and unpublished investigations of malignant pleural mesothelioma (cell lines, tumour specimens, animal models), with emphasis on work at the National Cancer Institute (USA) and collaborators
- Exposure: Asbestos fibres of two families, serpentine (chrysotile) and amphiboles (including crocidolite, amosite, tremolite); an SV-40-like virus was also discussed as a possible co-carcinogen
- Main results:
- The authors' group induced nitric oxide production in mouse (murine) macrophages by exposure to crocidolite fibres and interferon-gamma
- In the authors' karyotypic analysis of nine mesothelioma cell lines, all had abnormal karyotypes
- In the study of loss of heterozygosity on chromosome 3p in mesothelioma cell lines and tumours, no correlation was noted with asbestos exposure or survival
- In 52 of the authors' own snap-frozen mesothelioma specimens, p53 expression was found in 31 (60%)
- Mutational analysis found p53 alterations in only 2 of 25 specimens
- 60% of malignant pleural mesotheliomas resected at the NCI/NIH since 1990 contained SV-40-like DNA
- In a hamster model, mesothelioma cells expressing antisense IGF-1 receptor had significantly reduced growth in vitro and decreased tumorigenicity in vivo compared with cells expressing sense IGF-1 receptor
- The authors' conclusion: The authors concluded that carcinogenesis of malignant pleural mesothelioma is not completely understood, and that significant improvement in treatment will come from increased understanding of the tumour's cellular and molecular biology
Topics
The National Library of Medicine indexes this study under subjects our site covers: Mesothelioma.
Medical terms in this study, explained in our Lexicon: Pleural Mesothelioma, Carcinogenesis, Mesothelioma.
Related studies
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- Molecular and genetic changes in asbestos-related lung cancer — P. Nymark, H. Wikman, et al. (2008)
- Molecular genetics and mechanisms of apoptosis in carcinomas of the lung and pleura: therapeutic targets — L.R. Motadi, N.L. Misso, et al. (2007)
- Cytogenetic and molecular genetic changes in malignant mesothelioma — M. Musti, E. Kettunen, et al. (2006)
- The molecular basis of asbestos induced lung injury — D.W. Kamp, S.A. Weitzman (1999)
- Gene therapy for malignant pleural mesothelioma: present and future — Y. Tada, Y. Takiguchi, et al. (2008)
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Cited on this site
How to cite it
Cite the study
J.S. Donington, D.J. Mew, H.I. Pass. Malignant pleural mesothelioma: newer aspects of carcinogenesis, molecular genetics, and prospects for future therapies. Surgical Oncology 1995;4(4):175-85. doi:10.1016/s0960-7404(10)80034-9. PMID: 8528480.
Cite our summary
“Malignant pleural mesothelioma: newer aspects of carcinogenesis, molecular genetics, and prospects for future therapies.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/malignant-pleural-mesothelioma-newer-aspects-of-carcinogenesis.
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