6-ketoprostaglandin-f1-alpha and Carcinoma--Non-Small-Cell-Lung

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Carcinoma, Non-Small-Cell Lung; Cytochrome P-450 Enzyme System; Dinoprostone; Epoprostenol; Humans; Intramolecular Oxidoreductases; Lung Neoplasms; Neoplasm Proteins

108 cases of advanced non-small cell lung cancer (NSCLC) with Qi deficiency and blood stasis syndrome (QDBS) had been studied in this paper. It has been found that: (1) QDBS existed commonly in 60.2% of NSCLC patients. (2) QDBS patients had lowered immune function and blood hypercoagulating function, as compared with healthy persons. (3) The abnormal change of immunological indexes such as TC subgroup. TXB2, 6-keto-PGF1 alpha, fibrinogen and plasmin activity as well as hemorheological indices are important pathophysiological manifestation of QDBS. Thus, the principle of supplementing Qi and activating blood circulation combined with reducing phlegm and resolving masses should be emphasized in future research.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Carcinoma, Non-Small-Cell Lung; Diagnosis, Differential; Female; Fibrinogen; Humans; Immunity, Cellular; Lung Neoplasms; Male; Medicine, Chinese Traditional; Middle Aged; T-Lymphocyte Subsets; Thromboxane B2

The sensitivity of cancer patient macrophages from different anatomical sites to arachidonic acid metabolism was investigated in tumor cell cytotoxicity assays. Alveolar macrophages and peripheral blood monocytes from 13 non-small cell lung cancer patients, peritoneal macrophages and peripheral blood monocytes from 13 ovarian cancer patients, and comparable macrophages from control patients with nonmalignant lung or gynecological diseases were tested. Inhibitors of either the cyclooxygenase pathway or the lipoxygenase pathway together with specific metabolites of each pathway were used to evaluate how these different macrophage populations are regulated by eicosanoids. In addition, metabolic studies were performed to compare directly the arachidonic acid metabolism of macrophages obtained from these different anatomical locations. The results demonstrate that the peripheral blood monocytes from lung cancer and ovarian cancer patients and the peritoneal macrophages from ovarian cancer patients are sensitive to cyclooxygenase inhibition; this was not seen with comparable macrophages from the relevant control patients. Sensitivity to modulation by cyclooxygenase inhibition correlated with increased cyclooxygenase metabolism and with the capacity of prostaglandin to mediate suppression of tumoricidal function in these populations of cancer patient macrophages. In contrast, alveolar macrophages from cancer patients were not sensitive to either cyclooxygenase inhibition or to prostaglandin-mediated suppression. No such differential influences were revealed for the lipoxygenase pathway of arachidonic acid metabolism in any macrophage population tested. Thus, eicosanoids, particularly those of the cyclooxygenase pathway, can be a critical immunoregulatory feature of certain tumor microenvironments.

Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acid; Carcinoma, Non-Small-Cell Lung; Dinoprostone; Humans; Indomethacin; Lung Neoplasms; Macrophages; Masoprocol; Monocytes; SRS-A