Increase of oleic acid in erythrocytes associated with malignancies.

There is increasing evidence that essential fatty acids (EFA) may have a role to play in the aetiology of some types of cancer although their precise mode of action is unknown. Differences in the metabolism of EFA between patients with benign or malignant prostatic disease may help to elucidate their role in the latter. We have, therefore, measured the concentration of the essential fatty acids, and their metabolites, in the phospholipid fractions of both plasma and tissue, in patients with either benign or malignant prostatic disease. Comparison of the median concentration of fatty acids in each group (n = 10) revealed significant differences between them. The phospholipid component of total lipid was greater in malignant (P less than 0.04, unpaired t-test) than in benign tissue. The concentrations of linoleic acid (LA) and di-homo gamma linolenic acid (DGLA) in plasma and tissue were not different between the two groups of patients, but a significant reduction in arachidonic acid (ARA) (P less than 0.002, Mann-Whitney U-test) and docosapentaenoic acid (DPA) (P = 0.009) concentrations was observed in malignant tissue as compared to benign. Patients with malignant prostatic disease also had a significantly higher concentration of oleic acid in phospholipids from both plasma and prostatic tissue. The stearic to oleic acid ratio was similar in plasma but was significantly reduced in malignant tissue (P = 0.006). We suggest that the decreased arachidonic acid concentration in malignant tissue may be due to its increased metabolism, via the lipoxygenase and cyclooxygenase pathways to produce higher concentrations of eicosanoids, rather than an impairment in desaturase activity in situ.

Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Essential fatty acid distribution in the plasma and tissue phospholipids of patients with benign and malignant prostatic disease

Chaudry

McClinton²,

Moffat³

et al. 1991

“…It should be stated however, that elevated lipid levels may not be the result of dietary influences but may reflect some underlying metabolic disturbance associated directly with the disease or with some hormonal factor related to the disease. A recent study of membrane fatty acid composition in red cells obtained from patients with different types of cancer, including breast cancer, showed major differences in fatty acid profiles in the cancer group (Wood et al, 1985). It was suggested that such differences may reflect a fundamental defect in lipid metabolism associated with certain types of cancer.…”

Section: Discussionmentioning

confidence: 99%

Plasma lipids and prolactin in patients with breast cancer

Bani¹,

Williams²,

Boulter³

et al. 1986

Summary In a comparative study of pre-and postmenopausal women with benign and malignant breast disease, a number of differences were observed in circulating plasma prolactin and lipid concentrations. Plasma lipids, phospholipids, triglycerides, cholesterol and free fatty acids were all higher in blood obtained from breast cancer patients prior to surgery. HDL-Cholesterol levels were significantly lower in these patients. These differences remained when the patient groups were sub-divided according to menopausal status. Plasma prolactin concentrations were also found to be higher in cancer compared with non-cancer patients, this effect being more marked in premenopausal than in postmenopausal patients. Premenopausal patients with invasive or poorly differentiated disease had significantly higher prolactin levels than those with non-invasive disease. No correlations were found between plasma prolactin and any of the lipid fractions.

“…Fatty acid changes in malignancy Wood et al (1985) found increased desaturation of stearic (18:0) to oleic acid (18:1) in red cell membranes from patients with colorectal cancer, and a consequently decreased 18:0/18:1 ratio. We found a similar change in the plasma 18:0/18:1 ratio in the tumour-bearing mice, but the reverse in the liver and spleen.…”

Section: Discussionmentioning

confidence: 99%

“…The degree of saturation affects membrane fluidity and permeability (Schlager & Ohanian, 1980a); 18:0/18:1 is lower in red cell membranes from cancer patients (Wood et al, 1985); the latter ratio and 16:0/16:1 indicate delta-9-desaturase activity; the 18:2/20:4 ratio reflects delta-6-denaturase, elongase and delta-5-desaturase activities and eicosanoid production (Fulton, 1984;Hubbard et al, 1988); 20:3/20:4 reflects delta-5-desaturase activity; the n-6/n-3 ratio indicates tumour aggressiveness which is high when n-6 levels are low (Lanson et al, 1990). …”

mentioning

confidence: 99%

Changes in tissue fatty acid composition in murine malignancy and following anticancer therapy

Yazıcı

Tavares²,

Stamford³

et al. 1992

Summary We studied the mouse NC tumour, a subcutaneously transplanted adenocarcinoma originally of mammary origin. Measurements per g tissue were made of 17 fatty acids (FAs), the combined amounts of n-3, n-6, saturated, unsaturated, and total FAs, and of various FA ratios in the tumour, mammary tissue, spleen, liver and plasma. Compared with mammary tissue from normal mice, tumours of vehicle-treated controls had less of seven of the FAs and more of two FAs. Mice bearing the NC tumour often had changed (usually decreased) amounts of FAs in the 'normal' spleen, liver and plasma, but not in mammary tissue. Treatment with methotrexate (MTX) was studied alone and with indomethacin which can potentiate MTX cytotoxicity. Indomethacin 1.25 mg kg-' (INDO) increased the amounts of 3/17 tumour FAs and the unsaturated FAs, but reduced 9/17 FAs, the saturated and the unsaturated FAs in 'normal' mammary tissue, and usually had no effect on the FAs of other tissues. MTX 2 or 4 mg kg-' (MTX 2 or 4 mg) ± INDO in general partly restored (increased) the amounts of tumour FAs, and reduced the saturated/unsaturated FA ratio. In the 'normal' spleen and plasma also, but not in the liver, MTX 2 mg generally somewhat restored the FA composition. However, as in the liver, the spleen 20:4 and 22:6 (which form prostaglandins and lipid peroxides) did not increase in the presence of INDO. With MTX 4 mg, some of the plasma and liver FAs decreased, in contrast to the tumour. There was generally no evidence of MTX potentiation by INDO. These results are discussed in relation to carcinogenesis, cachexia, and the response to treatment.