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.