Imiquimod treatment of papilloma virus and DMBA /TPA-induced cutaneous skin cancer in Mastomys coucha: an unique animal model system useful for preclinical studies
Article first published online: 7 DEC 2007
DOI: 10.1111/j.1365-2133.2007.08266.x
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How to Cite
Nafz, J., Ohnesorge, M., Stockfleth, E., Rösl, F. and Nindl, I. (2007), Imiquimod treatment of papilloma virus and DMBA /TPA-induced cutaneous skin cancer in Mastomys coucha: an unique animal model system useful for preclinical studies. British Journal of Dermatology, 157: 14–17. doi: 10.1111/j.1365-2133.2007.08266.x
Publication History
- Issue published online: 7 DEC 2007
- Article first published online: 7 DEC 2007
- Accepted for publication 4 September 2007
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Keywords:
- animal models;
- epithelial skin cancer;
- imiquimod;
- keratoacanthoma;
- Mastomys coucha
Summary
Background Immune response modifiers including imiquimod can be topically applied for the treatment of both genital warts and benign and malignant skin tumours (e.g. actinic keratosis). In an initial pilot study, we examined the response of spontaneously papillomavirus caused skin lesions (e.g. papillomas, keratoacanthomas) vs. chemically induced skin tumours of Mastomys coucha to imiquimod.
Methods Fourteen spontaneously and 16 chemically [initiation with 7,12-dimethylbenzanthracene (DMBA) followed by repeated 12-O-Tetradecanoylphorbol-13-acetate (TPA) applications] induced skin tumours were treated two to three times per week with 5% imiquimod or placebo.
Results Notably, significant higher regression or growth arrest rates of imiquimod treated animals were observed in chemically vs. spontaneously induced skin tumours [9/14 (64%) vs. 2/11 (18%), P < 0·05]. Regression or growth arrest of both skin tumours from placebo treated animals were similar (1/2 vs. 1/3). Tumour growth of nonresponders was lowest in imiquimod treated animals compared to the placebo or untreated group.
Conclusions Imiquimod was able to reduce skin tumour growth particularly in chemically induced lesions of Mastomys coucha. The different clearance rates are most likely due to lower differentiation status of the DMBA/TPA-induced tumours, allowing a better uptake of imiquimod than spontaneously induced papillomas or keratoacanthomas, known to be highly keratinized.

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