Published in Cancer Detection and Prevention 1996; 20(5).
Evaluation of the model system for metastasis and cachexia in hamster cheek-pouch carcinomaDept 1Oral and Maxillofacial Surgery I; 2Oral Biochemistry, Matsumoto Dental College, Nagano 399-07, Japan
AIM: Early attempts to induce oral carcinoma in experimental animals were unsuccessful since the oral mucous is more resistant to the actions of chemical carcinogen than skin. Since Salley described hamster cheek-pouch (HCP) carcinoma induced by 9, 10-dimethyl-1,2-benzanthracene (DMBA) in 1954, this model system is an excellent experimental model for the study of pathology of oral cancer. However, there are a few reports about pathophysiological changes of the tumor-bearing host especially in cachexia. We tried to establish and evaluate the model of the lymph-node metastasis and tumor cachexia using HCP carcinoma. METHODS: Syrian golden hamster received three applications/week to the left HCP of 0.3% DMBA in acetone for 14 weeks and received no further treatment during next 6 weeks; 1) Model for metastasis: hamsters were divided into 5 groups: Control, excision of tumor, excision/Cortisone, excision/Cyclosporin-A, and excision/OK432 (immunopotentiator), and then the lymph-node metastasis was examined microscopically. 2) Model for cachexia: The sera (1ml once a week) from experimental hamsters were analyzed for several lipids: triglyceride, sialic acid, lipoprotein lipase (LPL) and TNF-alpha. RESULTS: 1) Metastasis rate: Control, 0%; excision, 43%; excision/Cortisone, 69%; excision/Cyclosporin-A 93%; and excision/OK432, 7%. 2) Tumor-bearing hamsters showed hyperlipidemia with cachexia, drastic reduction of LPL activity and the presence of TNF-alpha. CONCLUSION: HCP carcinogenesis provides a good model system to study metastasis and cachexia.
Paper presented at the International Symposium on the Impact of Cancer Biotechnology on Diagnostic and Prognostic Indicators; Nice, France; October 26 - 28, 1996; in the section on Metastasis.