Development of lung tumors in mutant p53-expressing mice after inhalation exposure to asbestos

Our plain-English summary of Development of lung tumors in mutant p53-expressing mice after inhalation exposure to asbestos, by G.F. Morris, A.R. Notwick, O. David, et al (Chest, 2004).

The study

• Authors: G.F. Morris, A.R. Notwick, O. David, C. Fermin, A.R. Brody, M. Friedman
• Journal: Chest
• Published: 2004;125(5 Suppl):85S-6S
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This brief conference report, from Tulane University Medical Center in New Orleans, described an experiment in mice on whether the tumor suppressor protein p53 protects against lung tumors caused by asbestos. The authors noted that the p53 gene is commonly mutated in human lung cancers but rarely in mouse lung tumors induced by carcinogen exposures. They had previously produced transgenic mice (SPC-DNp53 mice) that express a dominant-negative form of p53 specifically in the lung epithelium, using the human surfactant protein C promoter. Unexposed mice of this strain developed lung tumors at a low incidence and with delayed onset. The authors cited evidence that inhaled asbestos activates p53 expression at sites of fiber deposition and that asbestos exposure increases the risk of lung cancer about fivefold. They proposed that the p53-mediated response to asbestos protects against lung tumors. Transgenic mice and nontransgenic littermates were exposed at the same time to a single 5-hour aerosol of asbestos. The transgenic mice had a significantly higher incidence of lung tumors than their nontransgenic littermates. The report did not give the number of animals, the type of asbestos, the exposure concentration, or tumor counts. The authors concluded that compromised p53 function in the lung epithelium cooperates with asbestos in lung tumorigenesis.

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 short conference report, from researchers at Tulane University Medical Center in New Orleans, described an experiment in mice. The authors used genetically engineered mice, called SPC-DNp53 mice, that made a faulty ('dominant-negative') form of the p53 protein in the cells lining the lungs. The p53 protein normally acts as a tumor suppressor, meaning it helps guard against cancer. These engineered mice and their non-engineered littermates were exposed at the same time to a single 5-hour aerosol of asbestos. The report does not say which type of asbestos was used, what dose was given, how many mice were studied or how many developed tumors. The authors reported that the engineered mice had a significantly higher incidence of lung tumors than the non-engineered littermates exposed alongside them. The authors concluded that weakened p53 function in the lung lining cooperates with asbestos in the development of lung tumors. The report gives no tumor counts, percentages or statistical details.

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: Animal experiment in genetically engineered (transgenic) mice, published as a brief conference report
• Who was studied: Transgenic SPC-DNp53 mice, which make a dominant-negative form of p53 in the lung lining, compared with nontransgenic littermates exposed at the same time. Numbers of mice are not stated. The work was done at Tulane University Medical Center, New Orleans.
• Exposure: A single 5-hour exposure to an aerosol of asbestos. The fiber type and dose are not stated.
• Main results:
  • After the asbestos exposure, the SPC-DNp53 transgenic mice had a significantly higher incidence of lung tumors than the nontransgenic littermates exposed at the same time. No counts or statistics are given.
• The authors' conclusion: The authors concluded that compromised p53 function in the lung epithelium cooperates with asbestos in the development of lung tumors.

Topics

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

Medical terms in this study, explained in our Lexicon: Lung Cancer, Epithelium, Deposition, Asbestos Exposure, Tumorigenesis.

Related studies

• Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage — S.J. Kim, P. Cheresh, et al. (2016)
• Low Exposures to Amphibole or Serpentine Asbestos in Germline Bap1-mutant Mice Induce Mesothelioma Characterized by an Immunosuppressive Tumor Microenvironment — Y. Kadariya, E. Sementino, et al. (2024)
• Susceptibility of p53-deficient mice to induction of mesothelioma by crocidolite asbestos fibers — J.M. Marsella, B.L. Liu, et al. (1997)
• Loss of heterozygosity of chromosome 3p21 is associated with mutant TP53 and better patient survival in non-small-cell lung cancer — C.J. Marsit, M. Hasegawa, et al. (2004)
• Dose-dependent mesothelioma induction by intraperitoneal administration of multi-wall carbon nanotubes in p53 heterozygous mice — A. Takagi, A. Hirose, et al. (2012)
• Bayesian analysis of the rate of spontaneous malignant mesothelioma among BAP1 mutant mice in the absence of asbestos exposure — D.M. Nielsen, M. Hsu, et al. (2025)

Browse more research in Chest, or return to medical research.