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• W14697923 abstract "The hamster buccal pouch experimental model for oral cancer has proven to be a superior model for oral mucosal carcinogenesis and is now receiving wide attention as one of the better overall experimental models for carcinogenesis. The malignant tumors are epidermoid carcinomas that develop slowly, in response to polyaromatic hydrocarbon carcinogen application, and are preceded by a keratotic and dysplastic lesion comparable to human precancerous leukoplakia. The hamster lesions are indistinguishable histologically from human oral epidermoid carcinomas of the well-to-moderately differentiated variety, at both light microscopic and ultrastructural levels. Both animal and human lesions have similar metabolic markers, such asgamma glutamyl transpeptidase (GGT) and lactic dehydrogenase. The hamster carcinoma develops with the activation and expression of specific oncogenes, often similar to those expressed in human oral cancer. These include c-erbBl, H-ras, K-ras, and mutant p53. The hamster lesions are clearly visible at all times and can be counted and measured at different stages of development so that figures can be obtained for overall tumor burden. The hamster tumors are also closely related to immune control, as in humans. The hamster tumor development is enhanced by immunosuppressive drugs such as cortisone and methotrexate, and retarded by immunoenhancing agents such as levamisole or BCG." @default.
• W14697923 created "2016-06-24" @default.
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• W14697923 date "1995-01-01" @default.
• W14697923 modified "2023-09-24" @default.
• W14697923 title "Inhibition and Regression of Experimental Oral Cancer by Beta Carotene and Vitamin E: Emerging Concepts" @default.
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• W14697923 doi "https://doi.org/10.1007/978-1-4612-0237-0_19" @default.
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