Effect of Dietary Fat on Growth Kinetics of Transplantable Mammary Adenocarcinoma in BALB/c Mice<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

Abstract

The growth of mammary adenocarcinomas in BALB/c mice fed a diet containing 10% corn oil (CO), which has about 60% of its fatty acids as linoleate, was significantly greater than that for tumors in mice fed diets containing either 10% hydrogenated cottonseed oil (HCTO), which has no linoleate, or 10% CO plus 0.003% indomethacin (IM). The proportion of the tumor occupied by the various cell types was quantitated from histologic sections for 2 different mammary adenocarcinomas. At 2 weeks post implantation the degree of inflammatory cell (IC) infiltration of the first adenocarcinoma (tumor IX) did not account for the difference in tumor mass induced by dietary fat. This conclusion was confirmed by a study of a group of tumors arising from hyperplastic alveolar nodule transplants, which showed a similar dietary response but in which IC infiltration was minimal even in the largest tumors. Cell cycle parameters of tumor IX were determined by the fraction-of-labeled-mitoses (FLM) procedure. No differences were found in the duration of the G1, S, G2, or M phases of the cell cycle or the total cell cycle time in neoplasms from the CO and HCTO diet groups. The fraction of tumor cells dividing in neoplasms from the 2 diet groups was also identical. The only parameter that was significantly different was the rate of tumor cell loss when determined by both indirect (FLM) and direct [( 125I]iododeoxyuridine) methods. Tumor cell loss for adenocarcinomas from mice fed HCTO or CO plus IM was approximately twice that obtained for tumors from the CO-fed mice. These observations on tumor cell loss were discussed in terms of: the influence of dietary linoleate on the size of mammary tumors and the involvement of prostaglandins in this process.