The frequency of p53 immunostaining in asbestos-associated mesotheliomas and non-asbestos-associated mesotheliomas

Our plain-English summary of The frequency of p53 immunostaining in asbestos-associated mesotheliomas and non-asbestos-associated mesotheliomas, by F.G. Mayall, H. Goddard, A.R. Gibbs (Histopathology, 1993).

The study

• Authors: F.G. Mayall, H. Goddard, A.R. Gibbs
• Journal: Histopathology
• Published: 1993;22(4):383-6
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

It has been suggested that asbestos might have an important role in the development of p53 mutations in mesotheliomas. The objective of this study was to examine asbestos-associated mesotheliomas and non-asbestos-associated mesotheliomas to establish whether the frequency of p53 immunostaining and, by implication, p53 gene mutation is related to asbestos exposure. Immunopositivity for p53 was found in seven (44%) of the 16 mesotheliomas examined. The frequency was approximately the same in both the asbestos-associated mesotheliomas and the non-asbestos-associated mesotheliomas. It is concluded that the frequency of p53 immunostaining in mesotheliomas and, by implication, the frequency of p53 gene mutation is probably not related to asbestos exposure.

In plain English

This laboratory study, from Llandough Hospital and the University of Wales College of Medicine in Cardiff, UK, asked whether p53 staining in mesothelioma tumours differed between tumours linked and not linked to asbestos. The authors treated that staining as a usual sign of a p53 gene mutation. They searched archive records for 16 mesothelioma cases that had tumour biopsies taken during life and lung tissue from autopsy. Tumour sections were stained for p53. Asbestos fibres in the lung tissue (amosite, crocidolite, tremolite and chrysotile) were counted by electron microscopy and compared with ranges for 'unexposed' adults. Eleven cases were judged probably asbestos-associated and five probably not. In one case the count was borderline and its interpretation uncertain. Seven of the 16 tumours (44%) stained for p53, and the frequency was approximately the same in both groups. The authors noted that staining and gene mutation do not always go together. The authors concluded that the frequency of p53 staining, and by implication of p53 mutation, in mesothelioma is probably not related to asbestos exposure.

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 study of archived mesothelioma cases, comparing p53 immunostaining of tumour biopsies with lung asbestos fibre counts from autopsy tissue
• Who was studied: 16 mesothelioma cases found by searching archive records (Llandough Hospital, Penarth, and University of Wales College of Medicine, Cardiff, UK), each with a tumour biopsy taken during life and autopsy lung tissue available; years of the cases and tumour site (pleural or peritoneal) are not stated
• Exposure: Lung asbestos burden measured by transmission electron microscopy with energy dispersive X-ray analysis, given as millions of fibres per gram of dried lung for amosite, crocidolite, tremolite and chrysotile, and compared with ranges for 'unexposed' adults (0-1 for amosite, crocidolite and tremolite; 0-50 for chrysotile)
• Main results:
  • p53 immunostaining was found in 7 (44%) of the 16 mesotheliomas
  • The frequency of p53 immunostaining was approximately the same in the asbestos-associated and the non-asbestos-associated mesotheliomas
  • Based on fibre counts, cases 1 to 11 were classed as probably asbestos-associated and cases 12 to 16 as probably non-asbestos-associated
  • Among positive tumours, the amount of staining varied: in some, most tumour cell nuclei were positive; in others, positivity was less abundant
  • No anthophyllite or erionite was detected in any of the 16 cases
• The authors' conclusion: The authors concluded that the frequency of p53 immunostaining in mesotheliomas, and by implication the frequency of p53 gene mutation, is probably not related to asbestos exposure, and that p53 mutation in mesotheliomas is not carcinogen-specific
• Limitations the authors state:
  • p53 staining does not always reflect a p53 gene mutation: some tumours stain without a mutation
  • p53 gene mutations can be present without detectable staining
  • In case 1 the fibre count was borderline and its interpretation uncertain
  • Because everyone has low-level environmental asbestos exposure, the 'non-asbestos-associated' cases could in principle also be due to asbestos, though the authors judged this extremely unlikely
  • The speed and length of formalin fixation probably strongly affect how much p53 staining is seen

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: Mesothelioma, Asbestos Exposure.

Related studies

• The diagnosis of desmoplastic malignant mesothelioma and its distinction from fibrous pleurisy: a histologic and immunohistochemical analysis of 31 cases including p53 immunostaining — W.E. Mangano, P.T. Cagle, et al. (1998)
• Simian virus-40 large-T antigen binds p53 in human mesotheliomas — M. Carbone, P. Rizzo, et al. (1997)
• Gender comparisons in human lung cancer: analysis of p53 mutations, anti-p53 serum antibodies and C-erbB-2 expression — D.G. Guinee, W.D. Travis, et al. (1995)
• p53 protein accumulation in lung carcinomas of patients exposed to asbestos and tobacco smoke — K. Nuorva, R. Mäkitaro, et al. (1994)
• Mesotheliomas induced in rats by the fibrous mineral erionite are independent from p53 alterations — E.V. Kleymenova, G. Horesovsky, et al. (1999)
• p53, p21 and metallothionein immunoreactivities in patients with malignant pleural mesothelioma: correlations with the epidemiological features and prognosis of mesotheliomas with environmental asbestos exposure — R. Isik, M. Metintas, et al. (2001)

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