Abstract 1855: Maternal consumption of long chain omega 3 fatty acids decreases risk for mammary gland cancer in the female C(3)1 TAg mouse

Omega 3 fatty acids have been shown to reduce incidence and slow growth of mammary gland cancer in rodent models. Omega 3 fatty acids in the maternal diet are important for normal fetal brain, eye and nervous system development. Since exposure to dietary components during the critical developmental times of gestation and lactation may alter risk for mammary gland cancer in females, we tested whether exposure to increased levels of long chain omega 3 fatty acids (from fish oils) would be preventive or promotional to mammary gland cancer in the offspring. Normal SV40 female mice were fed AIN 76 diets containing either 10% corn oil (control) or 5% of an omega 3 fatty acid concentrate + 5% canola oil. Females were then mated with C(3)1 TAg transgenic mice. Transgene hemizygous offspring were the experimental mice not the original SV40 female mice. On a normal diet the hemizygous mice are expected to have about 100% tumor incidence by 150 days of age. At weaning (3 weeks) pups were randomized to either the corn oil or the fish oil diet, 15-17 mice per group. At 140 days of age, mice never exposed to fish oil (C/C group) had a significantly higher incidence and multiplicity of mammary gland tumors than mice exposed to fish oil throughout life (F/F group). Mice exposed to fish oil during a portion of life (C/F or F/C) had intermediate incidences and multiplicities. Interestingly, omega 3 in the maternal diet alone decreased tumor multiplicity by 50% compared to no omega 3, even when the mouse received a control diet after weaning. If a mouse, developed a tumor the mean tumor masses were not significantly different though the F/F group had a much smaller mean tumor mass. Adequate omega 3 fatty acids in the maternal diet may reduce risk for mammary gland cancer in the offspring. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1855. doi:10.1158/1538-7445.AM2011-1855