Summary 6-keto-PGFi,, and thromboxane B2 were determined by radioimmunoassay in 37 extracts of breast carcinomata, 8 fibroadenomata, 12 sclerocystic-disease specimens and 51 normal breast tissues. More prostanoids were extracted from carcinomata than from normal specimens, fibroadenomata or sclerocysticdisease tissues (P<0.05). The 6-keto-PGF1./TXB2 ratio was higher in carcinomata than in normal tissues and fibroadenomata (P<0.05) but was not significantly different from the ratio in sclerocystic disease. The prostaglandin levels and the 6-keto-PGF1./TXB2 ratios from carcinomata did not correlate significantly with age, tumour size, differentiation, lymph node status, nuclear-cytoplasmic ratio, host cell reaction, mast cells, necrosis, elastosis, fibrosis or blood vessel density. Lower nuclear density was associated with lower 6-keto-PGF1,/TXB2 ratios (P=0.01) whereas the latter value was higher when infiltration was lower (P=0.03). There was a positive correlation between mitotic index and the 6-keto-PGF1./TXB2 ratio (P=0.04).Cumulation of variables revealed lower prostanoid ratios in tumours >2cm without lymph node metastasis then tumours <2cm with lymph node metastasis (P=0.05). A first follow-up (14 months) showed a higher 6-keto-PGF1./TXB2 ratio in patients who developed metastasis (P=0.04). Our study does not confirm the hypothesis that high prostacyclin levels are a good prognostic index in breast cancer.Honn et al. (1981) found that prostacyclin (PGI2) had a beneficial influence against metastasis of B16 amelanotic melanoma tumours in mice, whereas inhibitors of PGI2 synthesis enhanced the number of metastases. Other authors tested the antimetastatic potency of acetylsalicylic acid, indomethacin, dipyridamole, flurbiprofen, benorylate, heparin and warfarin (Gasic et al., 1973;Elias et al., 1973;Lione & Bosman, 1978;Bennett, 1982). Most of these studies are done on animals and showed no clearcut results.Thromboxane (TX) A2 is often a physiological antagonist of PGI2 and an imbalance between them can disturb the (anti)haemostatic system. The antiaggregating properties of nonsteroidal antiinflammatory drugs (NSAID) can be explained by a stronger inhibition of the platelet cyclo-oxygenase in comparison with that of the vessel wall. As a result the release of TX will be lowered and aggregation will be blocked (Bunting et al., 1983). Sloane et al. (1981) showed that some tumours are able to release cathepsin B. This enzyme stimulates the synthesis of TX and is produced in a variant of B16 melanoma which has high metastatic activity.In order to study a possible prognostic value of the PGI2/TX ratio in breast cancer, the stable hydrolysis products of PGI2 (6-keto-PGF1,) and TXA2 (TXB2) were determined by RIA. 6-keto-PGF1, and TXB2 levels were examined in relation to the size of the tumour, axillary lymph node status, lymphatic vessel permeation, differentiation of the tumour, mitotic index density of nuclei of tumour cells, and age of the patient.PG production can be influenced by inflammatory processes (Humes...

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