TIME-COURSE STUDY OF ADIPOSE-TISSUE FATTY-ACID COMPOSITION DURING MAMMARY-TUMOR GROWTH IN RATS WITH CONTROLLED FAT INTAKE

Previous work in breast cancer patients has indicated an inverse relat ionship between the risk of relapse and the alpha-linolenic acid (18:3 n-3) level in adipose breast tissue. To determine whether low alpha-li nolenic levels in patients with aggressive breast cancer resulted from lower 18:3n-3 dietary intake and/or increased metabolism of stored 18 :3n-3, we analyzed the fatty acid composition of mammary adipose tissu e during tumor growth in a rat model of mammary carcinogenesis. Rats w ere fed a diet containing 10% fat as rapeseed oil (in which 9% of tota l fatty acids is 18:3n-3). One-half of the rats received an injection of nitrosomethylurea (NMU) to initiate mammary tumors. In control and NMU-treated groups, three to five animals were sacrificed every three weeks during the five-month experimental time. Tumor growth was follow ed by weekly palpation of the animals and by the measure of total tumo r mass and number in sacrificed rats. Mammary tumor and adipose tissue s were sampled in sacrificed rats.We found that although mammary adipo se tissue fatty acid profile changed throughout the experiment, there was no difference in fatty acid profile between control and NMU-treate d rats of the same age. In the NMU-treated group, 18:3n-3 level remain ed identical throughout the experimental period, irrespective of tumor burden. These data show that, in this model, mammary tumor growth doe s not modify stored fatty acid levels, including 18:3n-3. This suggest s that decreased 18:3n-3 level in patients with poor prognosis is not a consequence of tumor burden but more likely depends on decreased die tary intake.