Genetic factors in the aetiology of malignant mesothelioma

Our plain-English summary of Genetic factors in the aetiology of malignant mesothelioma, by M. Huncharek (European Journal of Cancer, 1995).

The study

• Author: M. Huncharek
• Journal: European Journal of Cancer
• Published: 1995;31A(11):1741-7
• Type of article: Review
• Cited by: 31 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This narrative review discussed what was then known about the genetic basis of malignant mesothelioma, a tumour whose incidence was rising. In the United States it rose from 0.6 cases per 100,000 in 1973 to 1.7 per 100,000 in 1984, an increase the author attributed largely to widespread asbestos exposure. The review first summarised reports of mesothelioma clustering within families, often with household or occupational asbestos exposure. It also covered studies of immune function and HLA type in asbestos-exposed people. It then reviewed flow cytometric studies, which found that mesotheliomas tended to be diploid or near diploid, for example 60 of 70 tumours (86%) in one series. In that series S-phase fraction, but not ploidy, was related to survival. Cytogenetic studies showed complex but recurrent losses or deletions involving chromosomes 1, 3, 6, 9 and 22. One series linked crocidolite and amosite exposure to loss of chromosomes 1, 3 and 4. Studies of oncogenes and tumour suppressor genes (c-sis, TP53, RB, NF2 and p16) were few. In one study p16 alterations were found in 39 of 40 cell lines and in 5 of 23 primary tumours. The author concluded that asbestos was the main cause of mesothelioma but that its carcinogenic mechanism remained unknown. He considered genetic susceptibility and family history worthy of further study and suggested that carcinogen-specific genetic markers could have public health and medico-legal implications.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This 1995 article was a narrative review by a single author of published research on genetic factors in malignant mesothelioma. It did not report new data of its own. The author reviewed reports of mesothelioma in several members of the same family. Many of these people had household or work exposure to asbestos, including a pair of identical twin brothers who had worked in a shipyard. The review also covered studies of immune function in asbestos workers, the DNA content of mesothelioma tumours, chromosome changes, and specific cancer-related genes such as TP53, NF2 and p16. According to the studies reviewed, mesotheliomas tended to be diploid or near diploid, and losses or deletions involving chromosomes 1, 3, 6, 9 and 22 recurred. In one reviewed study, 39 of 40 mesothelioma cell lines showed p16 alterations, compared with 5 of 23 primary tumours. The author noted that the role of oncogenes in mesothelioma was unknown and that data were limited. The author concluded that the reports of family clustering deserved more intense study.

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 new data)
• Who was studied: Published reports and studies, including case reports of families with several mesothelioma cases, immune studies of asbestos workers, and laboratory studies of mesothelioma tumour samples and cell lines
• Exposure: Asbestos in general. The reviewed reports involved occupational and household exposure, crocidolite and amosite in lung fibre analyses, and laboratory exposure of human mesothelial cells to amosite and chrysotile (with toxicity values also given for crocidolite)
• Main results:
  • Among the reviewed family reports was a pair of identical twin brothers, both shipyard workers, who developed pleural mesothelioma
  • From the ploidy studies reviewed, the author judged that mesotheliomas tend to be diploid or near diploid, unlike many other solid tumours
  • Across the reviewed cytogenetic studies, recurring losses or deletions involved chromosomes 1, 3, 6, 9 and 22
  • In a reviewed study by Tammilehto and associates of 41 mesothelioma cases, crocidolite and amosite were associated with loss of chromosomes 1, 3 and 4
  • In a reviewed study by Cheng and associates, 39 of 40 mesothelioma cell lines and 5 of 23 (22%) primary tumours showed p16 alterations
  • The author stated that the role of oncogene activation in mesothelioma was unknown
• The authors' conclusion: The author concluded that the sporadic reports of family clustering suggest genetic susceptibility deserves more intense study
• Limitations the authors state:
  • The author noted that only limited data exist on the prognostic value of S-phase fraction in mesothelioma
  • The author noted that very few studies have examined oncogenes in mesothelioma
  • The author noted that the cited TP53 studies gave no demographic information on the patients whose tumours were studied

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, Crocidolite, Amosite, Carcinogenic.

Related studies

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• The aetiology of mesothelioma: are risk factors other than asbestos exposure important? — R. Hubbard (1997)
• Malignant pleural mesothelioma: newer aspects of carcinogenesis, molecular genetics, and prospects for future therapies — J.S. Donington, D.J. Mew, et al. (1995)
• Endemic malignant mesothelioma: exposure to erionite is more important than genetic factors — M. Metintas, G. Hillerdal, et al. (2010)
• Are oestrogens and genetic predisposition etiologic factors in the development of clear cell carcinoma of the peritoneum? — R. Wuntakal, A. Lawrence (2013)

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