Failure to demonstrate tumour-associated transplantation antigens on asbestos-induced mesotheliomas in rats

Our plain-English summary of Failure to demonstrate tumour-associated transplantation antigens on asbestos-induced mesotheliomas in rats, by D.G. Brown, J.C. Wagner, M.M. Wagner (British Journal of Cancer, 1980).

The study

• Authors: D.G. Brown, J.C. Wagner, M.M. Wagner
• Journal: British Journal of Cancer
• Published: 1980;42(5):797-801
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

In plain English

This short communication reported a laboratory experiment in rats. The authors asked whether asbestos-induced mesotheliomas carry tumour-associated transplantation antigens (TATA), cell-surface markers that can let the immune system reject a tumour. PVG/C Norwegian hooded rats received 20 mg of UICC crocidolite injected into the chest cavity. Seven mesothelioma tumour lines were established and passed from rat to rat. Groups of rats were immunized either by having a tumour surgically removed or by receiving irradiated tumour grafts. They were then challenged with live tumour cells. Five tumours were not rejected at the minimum challenge dose under either method. In contrast, rats immunized against fibrosarcomas caused by the chemical 3-methylcholanthrene resisted at least four times the minimum dose of those fibrosarcoma cells needed to produce tumours in non-sensitized rats. The authors were satisfied that the rats' immune systems worked. They concluded that their work supported the idea that long-latent-period tumours do not stimulate rejection through TATA. They noted that negative results can arise from antigen loss or poorly timed challenge, and that the physical properties of asbestos must also be considered.

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 (short communication) testing tumour immunogenicity in rats using excision-challenge and irradiated-graft immunization regimes
• Who was studied: Syngeneic PVG/C Norwegian hooded rats (26 males and 17 females aged 6 to 7 weeks were injected to induce tumours), housed at the MRC Pneumoconiosis Unit, Penarth. Groups of 5 to 8 rats were used for each transplanted tumour.
• Exposure: Intrapleural injection of 20 mg of UICC crocidolite in 0.4 ml of saline. The resulting mesotheliomas were then transplanted into other rats. 3-methylcholanthrene-induced fibrosarcomas served as a positive comparison, and a spontaneous lung adenocarcinoma (ADC1) from a crocidolite-treated rat served as a control.
• Main results:
  • Seven mesothelioma tumour lines were established: 5 of male origin and 2 of female origin.
  • Five of the mesotheliomas were not rejected at the minimum tumour-cell dose in either the excision regime or the irradiated-graft regime.
  • Some resistance to the spontaneous adenocarcinoma (ADC1) was apparent.
  • For the 3-methylcholanthrene-induced fibrosarcomas, immunity to 4 x 10^5 Mc1 cells and 5 x 10^5 Mc3 cells was demonstrated. This represented resistance to at least a 4-fold increase above the minimum dose of those fibrosarcoma cells needed for tumour production in non-sensitized rats.
  • In the immunocompetence tests, ear thickness after BCG and PPD challenge was significantly greater than in the untreated ear (P less than 0.001). The authors were satisfied that immune competence was demonstrated both in vivo and in vitro.
  • The authors found no evidence of the strong rejection response that would support viral involvement (viral synergism) in producing mesotheliomas.
• The authors' conclusion: The authors concluded that their work supports the general concept that tumours with long latent periods are unable to stimulate host rejection through cell-surface expression of TATA.
• Limitations the authors state:
  • The authors noted, citing others, that negative results may arise from too little or the wrong kind of antigen expression, from antigen loss or modulation, or from challenging with tumour cells at the wrong time relative to peak immunity.
  • The authors stated that equal consideration must be given to the fact that the carcinogen used (asbestos) has important physical properties.

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.

Related studies

• Frequency of HLA antigen in asbestos workers with and without pulmonary fibrosis — C.C. Evans, H.C. Lewinsöhn, et al. (1977)
• Expression of the small cell carcinoma antigens of cluster-5 and cluster-5A in primary lung tumours — A. Maier, U. Schmidt, et al. (1989)
• Diagnosing tumours on routine surgical sections by immunohistochemistry: use of cytokeratin, common leucocyte, and other markers — R.N. Poston, Y.S. Sidhu (1986)
• Tumor-infiltrating dendritic cells exhibit defective cross-presentation of tumor antigens, but is reversed by chemotherapy — A.M. McDonnell, W.J. Lesterhuis, et al. (2015)
• Experimentally induced mesothelioma in white rats in response to intraperitoneal administration of amorphous crocidolite asbestos: preliminary report — K. Kolev (1982)
• P53 mutations in tumours induced by intraperitoneal injection of crocidolite asbestos and benzo[a]pyrene in rats — K. Unfried, N. Kociok, et al. (1997)

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