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Plasmacytoma development in mice injected with silicone gels
1Laboratory of Genetics, DCBDC, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA.
Current Topics in Microbiology and Immunology
|January 1, 1996
Summary
Silicone gels from implants cause plasmacytomas in susceptible mice, unlike silicone oils. Gels induce inflammation, suggesting unknown components trigger tumor formation, while oils do not.
Area of Science:
- Biomedical research
- Materials science
- Immunology
Background:
- Silicone implants are widely used in medical devices.
- The potential for silicone materials to induce adverse biological reactions requires investigation.
- Previous studies have not fully elucidated the tumorigenic potential of different silicone formulations.
Purpose of the Study:
- To investigate the tumorigenic potential of silicone gels and silicone oils in a susceptible mouse model.
- To compare the biological effects of silicone gels versus silicone oils.
- To identify potential components within silicone gels responsible for tumor induction.
Main Methods:
- Administration of silicone gels and dimethylpolysiloxane (DMPS) silicone oils to BALB/cAn.DBA/2-Idh1-Pep3 congenic mice.
- Monitoring for plasmacytoma formation and associated inflammatory responses.
- Histopathological analysis of induced lesions.
Main Results:
- Silicone gels induced plasmacytomas in 60-70% of susceptible mice.
- Dimethylpolysiloxane (DMPS) silicone oils and vinylmethylpolysiloxane did not elicit tumors.
- Silicone gels, but not oils, induced a significant inflammatory silicone granuloma.
- The specific chemical component in gels responsible for tumor induction remains unidentified.
Conclusions:
- Silicone gels, distinct from silicone oils, possess tumorigenic properties in susceptible mice.
- The inflammatory response induced by silicone gels may create a permissive environment for plasmacytoma development.
- Further research is needed to identify the specific chemical agents within silicone gels responsible for oncogenesis.