Increased synthesis of prostacyclin and thromboxane in human ovarian malignancy
To study the production of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane (TxA2) by ovarian tumors, we incubated pieces of benign and malignant ovarian tissue in vitro, and measured by radioimmunoassay the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (a hydration product of PGI2) and thromboxane B2 (TxB2) (a hydration product of TxA2). Healthy ovary (n = 10) produced both 6-keto-PGF1 alpha [mean, 8.9; 95% confidence interval (CI) from 5.4 to 15.2 ng/mg
... o 15.2 ng/mg protein/min] and TxB2 (mean, 1.9 ng/mg protein/min; 95% CI from 1.0 to 3.7 ng/mg protein/min). The production of 6-keto-PGF1 alpha (mean, 12.2; 95% CI from 7.7 to 19.3 ng/mg protein/min) and that of TxB2 (mean, 4.8; 95% CI from 2.1 to 11.9 ng/mg protein/min) by benign cystic tumors (n = 12) was normal. Ovarian anaplastic cancer and adenocarcinoma (n = 12) produced 6-keto-PGF1 alpha on average 11.6-fold (95% CI from 5.2 to 26.0) 6-keto-PGF1 alpha and TxB2 on average 30.0-fold (95% CI from 13.5 to 66.7) over production by healthy ovaries, and the ratio of 6-keto-PGF1 alpha to TxB2 shifted to the dominance of TxB2. Similarly ovarian metastases of breast cancer, tubal cancer, and colon cancer produced increasingly 6-keto-PGF1 alpha (mean, 20.7 ng/mg protein/min) and TxB2 (5.1 ng/mg protein/min). The dominance of TxA2 in human ovarian cancer may contribute to the aggressing growth and spreading of this tumor.