Decreased stabilization of prostacyclin activity in patients with bone tumors.
Tumor metastasis is mediated in part by platelet activation. Since prostacyclin regulates platelet activity, we examined stabilization of bioactivity of exogenous prostacyclin in plasma of patients with malignant bone tumors. Bioactivity of prostacyclin (platelet aggregation inhibition) incubated in patient plasma was found to be significantly less compared to that in normal plasma. In addition, the duration of bioactivity of prostacyclin was considerably less in plasma of patients with bone tumors. These preliminary data indicate decreased prostacyclin activity in plasma of patients with malignant bone tumors, which may be a mechanism of platelet-tumor cell aggregate formation and subsequent evolution of metastasis.
D000293:Adolescent; D000328:Adult; D001859:Bone Neoplasms / Q000097:blood*; D002648:Child; D011464:Epoprostenol / Q000097:blood / Q000494:pharmacology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009362:Neoplasm Metastasis; D012516:Osteosarcoma / Q000097:blood*; D010974:Platelet Aggregation / Q000187:drug effects*; D012016:Reference Values; D012512:Sarcoma, Ewing / Q000097:blood*
D011464:Epoprostenol