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KMID : 0355619950210020132
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Journal of Korean Association of Oral and Maxillofacial Surgeons
1995 Volume.21 No. 2 p.132 ~ p.148
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Immunohistochemical study of p53 GENE,EGF-gamma and pcna in DMBA induced hamster buccal pouch carcinogenesis model
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Abstract
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This study was carried out to investigate the cellular and molecular mechanisms of hamster buccal pouch carcinogenesis treated with 0.5% DMBA (7,12-dimethylbenz[a]anthracene) in mineral oil.
Ninety two Syrian golden hamsters, maintained on a stock diet, 4-6 weeks old, were diveded into control and 3 experimental groups(20 hamsters), were left untreated on both buccal pouches of hamsters. Animals were sacrificed at 0, 4, 8 and 16
weeks.
Experimental groups (72 hamsters), were treated with 0.5% DMBA tri-weekly on the right buccal pouch. Animals were sacrificed at 4, 8, 16 weeks after treatment. Sacrificed animal buccal pouches were sectioned and examined for potential alterations
in the
expression of p53 tumor suppressor gene to determine whether p53 alterations are modulated in the different stages of hamster buccal pouch carcinogenesis. For these samples, we also investigated the expression patterns of EGF-r (epidermal growth
factor
receptor). PCNA (proliferating cell nuclearantigen) was used to investigate cell kinetics of hamster tumors.
@ES The results were as follows :
@EN 1. The DMBA-treated buccal pouches were generally white and irregularly thickened up to 8 weeks. There were multiple, various polypoid tumors throughout the mucosa at 16 weeks. Light microscopically the buccal pouch epithelium in DMBA-treated
groups
showed areas of hyperkeratosis and hyperplasia at 4 weeks, dysplasia at 8 weeks, and early and invasive squamous cell carcinoma at 16 weeks.
2. The presence, pattern and distribution of p53 staining depended greatly on the morphology of the lesion. The non-neoplastic lesions were negative for mutant p53 protein, whereas preneoplastic (hyperplasia and dysplasia) and neoplastic lesions
(squamous cell carcinoma) were positive for p53.
3. EGF-r expression was found in non-neoplastic and preneoplastic lesions, but no expression in the neoplastic lesion.
4. The PCNA labeling index correlated well with the stages of buccal pouch epithelium carcinogenesis.
5. The staining pattern and distribution for mutant p53 protein was directly correlated with PCNA distribution whereas neither directly correlated with EGF-r.
These results suggest that p53 alterations occur in a multistep fashion with corresponding increase of cell kinetics revealed by PCNA during the hamster buccal pouch carcinogenesis. Mutation of the p53 gene is an important step in the
pathogenesis
of
DMBA-induced hamster buccal pouch squamous cell carcinoma but EGF-r expression may be incidental.
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KEYWORD
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