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Increased Synthesis of Prostacyclin and Thromboxane in Human Ovarian Malignancy¹

First Department of Obstetrics and Gynecology [A. M. A-T., R. O. Y.] and Children's Hospital [L. U. V.], University of Helsinki, SF-00290 Helsinki, Finland

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 F_1a (6-keto-PGF_1a) (a hydration product of PGI₂) and thromboxane B₂ (TxB₂) (a hydration product of TxA₂). Healthy ovary (n = 10) produced both 6-keto-PGF_1a [mean, 8.9; 95% confidence interval (CI) from 5.4 to 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-PGF_1a (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-PGF_1a on average 11.6-fold (95% CI from 5.2 to 26.0) 6-keto-PGF_1a and TxB₂ on average 30.0-fold (95% CI from 13.5 to 66.7) over production by healthy ovaries, and the ratio of6-keto-PGF_1a to TxB₂ shifted to the dominance of TxB₂. Similarly, ovarian metastases of breast cancer, tubal cancer, and colon cancer produced increasingly 6-keto-PGF_1a (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.

¹ This study was supported by grants from The Finnish Academy of Science, the Cancer Research Foundation, and the Sigrid Juselius Foundation.

² To whom requests for reprints should be addressed, at Department of Obstetrics and Gynecology, University of Helsinki, Haartmaninkatu 2, SF-00290 Helsinki, Finland.

Received 6/ 9/87. Revised 12/ 8/87. Accepted 1/22/88.

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