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Differential Effects of Dietary Linoleic Acid on Mouse Skin-Tumor Promotion and Mammary Carcinogenesis¹

University of Texas M.D. Anderson Cancer Center, Science Park, Research Division, Smithville, Texas 78957 [S. M. F., J. L., M. L. L., R. E. M., T. J. S.]; University of Texas at Austin, Division of Nutrition, Austin, Texas 78712 [M. L., M. A. B.]; and Best Foods, Inc., Research and Engineering Center, Union, New Jersey 07083 [D. H. B.]

On the basis of reports of rat mammary- and pancreas-tumor models, we hypothesized that an increase in consumption of linoleic acid (LA) would also cause an enhancement in mouse skin-tumor promotion. SENCAR mice were placed on diets containing 0.8%, 2.2%, 3.5%, 4.5%, 5.6%, 7.0%, or 8.4% LA, 1 week after initiation with 7,12-dimethylbenz(a)anthracene and 3 weeks before starting promotion with 12-O-tetradecanoylphorbol-13-acetate. An inverse correlation (r = -0.92) was observed between papilloma number and level of LA; however, there was little difference in tumor incidence. A relationship between diet and carcinoma incidence was also found. The fatty acid composition of epidermal phospholipids reflected the dietary LA levels. 12-O-Tetradecanoylphorbol-13-acetate-induced epidermal prostaglandin E₂ levels generally decreased with increasing dietary LA. To determine whether this inverse correlation between dietary LA and tumor yield was due to species differences or organ-model differences, a mammary carcinogenesis experiment was performed. SENCAR mice were fed the 0.8%, 4.5%, and 8.4% LA diets. All mice received 6 mg 7,12-dimethylbenz(a)anthracene, administered intragastrically at 1 mg/week. Tumor appearance was delayed in the 0.8% LA diet group, and a positive dose-response relationship between dietary LA and mammary-tumor incidence was observed. These studies suggest that the effect of dietary LA on tumor development is target tissue specific rather than species specific.