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rcoma transplanted in protein-depleted rats. Ross and Bras in 1971 reported a reduced incidence of spontaneous benign and malignant tumors in COBS rats with underfeeding. This pattern of tumorigenesis was established early in life in this model and remained stable with subsequent nutrient alterations.
     Nutrient administration can also effect the growth of carcinogen - induced tumors. White in 1961 reviewed numerous carcinogen-induced malignancies in mice and rats and reported that protein-calorie deprivation reduced the incidence of such malignancies. Moore and Tittle documented similar findings in dimethylbenzanthracene-induced breast tumors in Sprague- Dawley rats. Thus, it is clear in numerous animal models that protein-calorie restriction is associated with a decreased incidence of spontaneous and carcinogen-induced tumors, inhibition of primary tumor growth and decreased establishment of transplanted tumors.
     Few clinical studies have been reported to corroborate these finding in-patients. Numerous associations have been made between high caloric intake, high fat intake and obesity, and the development of several human tumors. In particular, hormone-sensitive tumors such as breast carcinoma, ovarian carcinoma, and colorectal cancer are associated with these nutritional factors. This rationale forms the basis for the development of current chemoprevention trials, which have been designed to determine the effect of specific external interventions on the incidence of human malignancies. Furthermore, these findings have led to the general recommendations of the American. Cancer Society and National Cancer Institute that decreased fat intake and increased fiber intake may be associated with reduced incidence of human tumors.

PRIMARY TUMOR GROWTH AND METASTASIS
     Animal Models
     Numerous tumor-bearing animal studies have demonstrated that tumor growth and metastasis can be significantly stimulated during periods of nutrition support. Tumor volume, tumor weight, cellular mitotic index, DNA, RNA, and protein synthesis and cell cycle changes have been used as parameters of tumor growth. Both oral and intravenous routes of nutrient administration have been associated with alterations of tumor growth.
     In 1976, Cameron and Pavlat compared total parenteral nutrition (TPN) with oral diets and studied growth of the Monis hepatoma in Buffalo rats. A 2 - week period of parenteral nutrition resulted in increased tumor volume, increased tumor mitotic index, and increased tumor: host weight ratio in this model. Using this same tumor system, Cameron in 1981 demonstrated a dramatic increase in H-thymidine lageling index of tumor cells after initiating total parenteral nutrition. Daly et al in 1978 compared with the restricted diet, the oral protein and carbohydrate diet and TPN caused an increase in tumor volume but with no change in the tumor: host weight ratio. Thus, there was stimulation of tumor growth but not out of proportion to host weight gain. In
the Walker 256 carcinosarcoma model in Sprague-Dawley rats, change from a restricted to oral     protein/carbohydrate diet resulted in an increase in tumor volume after only 48 hours of this change.
     Parenteral nutrients were similarly found to accelerate tumor growth in additional tumor m