The first evidence that dietary fat influences mammary carcinogenesis was provided by Tannenbaum, who showed that mice fed a high-fat diet developed spontaneous tumors more readily than those fed a low-fat diet. Similar observations have been made with various other animal models. Polyunsaturated vegetable oils enhance carcinogenesis more effectively than saturated fats, because of their higher linoleate content. Diets containing high levels of polyunsaturated fish oils do not stimulate carcinogenesis, however, perhaps because their polyunsaturated fatty acids belong mainly to the linolenate family. Dietary fat acts primarily as a promoting agent, but the exact mechanism is still unclear. The requirement for linoleate and the fact that the fat effect can be blocked by prostaglandin biosynthesis inhibitors suggests that it may be mediated by biologically-active compounds derived from linoleate. Other possibilities include changes in hormonal balance, alterations in the fatty acids of membrane lipids, effects on the immune system, modulation of intercellular communications, and metabolic alterations related to differences in fat and caloric intake. Interest in the role of dietary fat in mammary carcinogenesis has been greatly stimulated by epidemiological evidence of a strong, positive correlation between breast cancer and dietary fat. In these epidemiological data, total dietary fat shows a better correlation than fat from either plant or animal sources individually, and there is no apparent correlation with the polyunsaturated fatty acid content of the diet. Further studies are needed to investigate more thoroughly this apparent difference between experimental and epidemiological data.(ABSTRACT TRUNCATED AT 250 WORDS)