Hyaluronan accumulates in ascites during intraperitoneal proliferation of TA3/St murine mammary carcinoma cells and at sites of their invasion of the peritoneal wall. To determine whether hyaluronan is functionally involved in these eventsBreast cancer cells metastasize directly through the vasculature to organs distant from the original tumor site, but they also invade and exfoliate into body cavities, especially the pleural space, where they grow in suspension within effusions.1 The rapid accumulation of these effusions is believed to result from increased permeability of the vasculature lining such cavities under the influence of tumor cell products, eg, vascular endothelial growth factor.2 The breast cancer cells eventually attach to and invade tissues lining the cavity wall. The tumor cells then gain access to the many blood vessels contained therein, leading to further dissemination of malignant cells to other organs. 3In a past study, we showed that hyaluronan accumulates in the ascites, and at initial sites of attachment and invasion of tumor cells at the mesothelial surface of the peritoneal wall, after introduction of murine ovarian tumor cells or mammary carcinoma cells into the peritoneal cavity of syngeneic mice. 4 Several types of malignant solid tumors contain elevated levels of hyaluronan, a ubiquitous glycosaminoglycan that contributes both to the structure of extracellular matrix and to cell-matrix interactions that influence cell behavior. 5,6 The enrichment of hyaluronan in tumors can result from increased production by tumor cells themselves 7,8 or from interactions between tumor cells and surrounding stromal cells that induce increased production by the latter.9 -11 High levels of hyaluronan correlate with tumor spread and with poor survival rates in human patients with a variety of tumor types, 12-15 and experimental evidence in animal models directly implicates hyaluronan in solid tumor progression. 16 -20 In the present study our objective was to determine whether hyaluronan also contributes to ascites growth and tumor cell invasion of the peritoneal wall.We have shown that stable transfection of TA3/St murine mammary carcinoma cells with cDNA encoding soluble CD44 prevents formation of metastatic nodules in the lung after introduction of the TA3/St cells into the vasculature. 17 In that study, soluble CD44 presumably acted as a competitive inhibitor of crucial hyaluronanprotein interactions because transfection with mutant soluble CD44 that does not bind hyaluronan had no effect Address reprint requests to Bryan P.

To assess cross-cultural relations between dietary intake and plasma lipoproteins, we randomly selected 222 men and 243 women from the urban and rural areas of Puriscal, Costa Rica; related their dietary composition (assessed by a food-frequency questionnaire), fitness level, and body fat to plasma lipids, apolipoproteins, and low density lipoprotein (LDL) particle size; and compared these data with those from a subsample of 280 adults from the Framingham Offspring Study. Total cholesterol and LDL cholesterol levels were significantly (p<0.0001) higher in Framingham (207 and 137 mg/dl, respectively) than in Puriscal (184 and 114 mg/dl, respectively) residents. Elevated triglyceride and apolipoprotein (apo) B levels (25% and 16% higher), low HDL cholesterol and apo A-I levels (12% and 29% lower), and smaller LDL particles (17%) were more frequent in Puriscal than in Framingham residents. Urban Puriscal residents had a significantly lower fitness level; increased body fat, total cholesterol, and triglyceride levels; decreased HDL cholesterol in men; and higher apo B levels in women compared with rural Puriscal residents. Body fat, animal fat, and saturated fat intakes were significantly correlated with total cholesterol, LDL cholesterol, and apo B levels in both men and women in Puriscal. Intakes of protein and animal fat were higher among urban (10.7% and 14.1%, respectively) compared with rural (8.9% and 9.9%, respectively) Puriscal residents and in Framingham (16.0% and 20.8%, respectively) compared with Puriscal residents. No significant differences were found in dietary cholesterol. Saturated fat (largely from palm oil in Puriscal) intakes were significantly different among the three groups: rural Puriscal, 10.7% of calories; urban Puriscal, 11.6%; and Framingham residents, 12.9%. These data indicate that the more atherogenic plasma lipid profile among urban compared with Puriscal residents was largely explained by increased adiposity, decreased fitness level, and higher saturated fatty acid intake. Puriscal residents consumed less animal fat and more carbohydrate than did Framingham residents, and these differences were associated with a 21% lower LDL cholesterol level, a 12% lower HDL cholesterol level, a 29% lower apo A-I level, a 25% higher triglyceride level, a 16% higher apo B level, and a 17% smaller LDL particle size. Some of these cross-cultural differences may be due to differences in ethnic background and physical activity as well. (Arteriosclerosis and Thrombosis 1991;ll:1089-1099)

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