Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin K deficiency, either dietary or pharmacologically induced by warfarin, was unable to affect the metastatic capacity of cells from a benzopyrene-induced fibrosarcoma in C57BL/6J mice. The same cells had a procoagulant activity, of tissue thromboplastin type, which was also completely unaffected by vitamin K antagonism or deficiency. In another murine model of spontaneous metastasis we previously suggested that depression of a particular procoagulant such as a direct factor X activator might contribute to the antimetastatic activity of warfarin. The failure of vitamin K deficiency to affect both the procoagulant and the metastatic capacity of the model reported here offers strong negative support to the same concept.
Eur J Cancer Clin Oncol 1985 Feb
PMID:Failure to warfarin to affect the tissue factor activity and the metastatic potential of murine fibrosarcoma cells. 398 61

In most reviews of arterial embolism or thrombosis the source of emboli or the cause of thrombosis can reasonably be established in over 90% of patients. Still about 10% remain without demonstrable cardiac or intraarterial sources. Although hypercoagulability induced by malignancy has been alluded to as a cause of unexplained intravascular thrombosis reports of arterial thromboembolism with such association are rare. Seven patients with unequivocal thromboembolism are presented. Two distinct clinical patterns are observed, one with in situ thrombosis of small arteries and the other with occlusion of large arteries causing limb ischemia or fatal organ infarction. The various pathogenetic mechanisms of arterial thrombosis or embolism in malignancy include sustained spasm of arteries, precipitation of cryoglobulins or other abnormal proteins in small arteries, direct tumor invasion of arteries, fragmentation and embolization of intracardiac or intraarterial metastases and spontaneous arterial thrombosis due to hypercoagulability. The hypercoagulable state can be recognized by the observation of shortened bleeding and clotting times, partial thromboplastin and prothrombin times, elevation of coagulation factors, platelets and yield stress index and resistance to anticoagulation. Patients presenting with arterial thromboembolic events with out demonstrable source should be investigated for malignancy. Conversely patients with malignancy should be searched for evidence of hypercoagulability in an attempt to prevent arterial thromboembolic complications.
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PMID:Arterial thrombosis and embolism in malignancy. 403 Aug 80

Prothrombinase affects the proteolytic conversion of prothrombin to thrombin and is the penultimate enzyme in the common coagulation pathway. Prothrombinase is a complex in which the proteinase, Factor Xa, a cofactor, Factor Va, and calcium are bound to a membrane surface to generate the active enzyme. Guinea pig line 1 and line 10 tumor cells, grown as primary cultures from ascites tumors or as cell lines in culture, provide a surface that interacts with coagulation Factor Va and Xa and with calcium ions to form this enzyme complex. Cultured human colorectal carcinoma cells (Colo 205) also participate in prothrombinase complex assembly and function. Prothrombinase generation was measured by following the kinetics of prothrombin conversion to thrombin. Thrombin generation was monitored continuously using the reversible thrombin inhibitor, dansylarginine N-(3-ethyl-1,5-pentanediyl)amide, which displays enhanced fluorescence upon binding to thrombin. Analyses of kinetic data indicate that the apparent dissociation constants (1-4 X 10(-10) mol/liter) and the number of Factor Va-Xa binding sites per tumor cell are comparable to values reported for human and bovine platelets, human lymphocytes, and monocytes. Guinea pig lymphocytes were also active, while erythrocytes were inactive, in the prothrombinase assay. Membrane vesicles, shed by guinea pig and human tumor cells into conditioned medium, also supported functional prothrombinase activity. Although earlier studies indicated that tumor cells may initiate coagulation, this is the first demonstration that tumor cells are competent to bring clotting to fruition by generating thrombin, a step essential to fibrin generation. These data suggest that tumor cells, in the presence of clotting initiators and appropriate coagulation factors, are sufficient to generate the fibrin deposited in solid tumors.
Cancer Res 1985 Nov
PMID:Tumor cell generation of thrombin via functional prothrombinase assembly. 405 25

A peritoneovenous (PV) shunt was placed in eight patients with intractable malignant ascites. The shunt successfully controlled the ascites in six patients. The median survival time of the entire group was 2 months, with one patient alive at 22 months. Two of seven patients had secondary shunt failure: one from an unknown cause which could not be corrected by revision and another which was corrected by revision following removal of psammoma bodies in the valve. The complications of the shunt included transient edema (four patients), transient intravascular coagulation (four patients), and fever (two patients). Tumor embolization was suspected pathologically in two of eight patients although the ascitic fluid contained malignant cells in seven of eight patients. The PV shunt is a satisfactory palliative procedure for malignant ascites in the presence of adequate cardiac function and in the absence of urinary obstruction. The presence of bloody effusion or major intra-abdominal mass lesions contra-indicates a successful PV shunt. The acute adverse effets of the PV shunt (fever, fluid overload, and fulminant disseminated intravascular coagulation) may be prevented or minimized by preoperative fluid removal to obviate a major intravascular infusion of colloid and biologically active pyrogen and thromboplastin.
Cancer Treat Rep
PMID:Complications of peritoneovenous shunt for malignant ascites. 615 65

Thirteen of 14 tumor cells or tumor cell lines of guinea pig, mouse, and human origin spontaneously shed procoagulant activity in short-term (4 or 14 to 22 hr) tissue culture under conditions of high cell viability. This released procoagulant activity was pelletable in the ultracentrifuge and was associated with plasma membrane-derived vesicles as determined by transmission electron microscopy and marker enzyme analysis. The procoagulant activity shed corresponded to a substantial fraction of that expressed by intact or sonicated tumor cells and was composed of activities interacting at more than a single step in the clotting sequence. One procoagulant activity associated with shed human tumor vesicles behaved as tissue factor, requiring Factor VII for activity and being inhibited by a specific anti-bovine tissue factor antibody. Guinea pig tumor vesicles also exhibited tissue factor-like activity in a two-stage assay using homologous first-stage Factor VII/X concentrate. None of the human vesicles tested expressed a direct Factor X cleaving activity, independent of Factor VII. Shed tumor vesicles also acted at a second step late in the clotting cascade at the level of prothrombinase generation, presumably by providing a phospholipid surface. Taken together, these data indicate that a wide variety of tumor cells release plasma membrane vesicles with procoagulant activity. Such vesicles, as well as intact tumor cells themselves, may play an important role in the biology of tumor growth by inducing the local fibrin deposits found in association with many solid tumors.
Cancer Res 1983 Sep
PMID:Procoagulant activity associated with plasma membrane vesicles shed by cultured tumor cells. 634 72

Cancer cells may promote fibrin formation in the tumor microenvironment through availability of procoagulant activities which are mainly of two types: tissue thromboplastin-like or direct activator of coagulation factor X. The pharmacological modulation of these activities could be potentially important in the control of metastasis growth. However, very limited information is available so far on this issue; it has recently been shown that the direct activator of coagulation factor X is a vitamin K-dependent activity which is depressed by warfarin treatment, not by anticoagulation with heparin or defibrinating enzymes. Whether the inhibition of this peculiar cancer procoagulant is involved in the antimetastatic activity of warfarin is a stimulating hypothesis which needs to be further substantiated.
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PMID:Cancer cell procoagulants and their pharmacological modulation. 639 43

The importance of the blood coagulation sequence as an integral part in the pathogenesis of diseases inside as well as outside the blood vessels is becoming increasingly apparent. Mononuclear phagocytes have important functions in initiation of coagulation by producing several procoagulant substances, including thromboplastin, the potent trigger of the extrinsic pathway. Increasing evidence demonstrates the clinical importance of monocyte and macrophage thromboplastin synthesis in the pathogenesis of a variety of diseases. This review surveys the role of monocyte/macrophage thromboplastin in relation to inflammatory diseases, cancer, disseminated intravascular coagulation and diseases of the blood vessels, thrombosis and atherosclerosis.
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PMID:Clinical significance of increased thromboplastin activity on the monocyte surface--a brief review. 639 44

The clinical and laboratory effects of low-dose heparin prophylaxis was prospectively studied in a controlled trial of 182 patients undergoing major surgery for gynecologic malignancy. Low-dose heparin was given in 5000 U subcutaneously two hours preoperatively and every 12 hours for seven days postoperatively. Low-dose heparin-treated patients had a significantly increased daily retroperitoneal hemovac drainage. Although not statistically significant, low-dose heparin was associated with increased estimated intraoperative blood loss, transfusion requirements, and wound hematomas. Fifteen percent of patients receiving low-dose heparin were found to have an activated partial thromboplastin time greater than 1.5 times the control value. In these patients, all clinical bleeding parameters were significantly increased. Low-dose heparin-treated patients also had significantly prolonged activated partial thromboplastin time and lower final platelet counts as compared with the control patients. When using low-dose heparin for thromboembolism prophylaxis, patients should be closely observed for clinical hemorrhagic complications. Activated partial thromboplastin times and platelet counts should be monitored throughout therapy.
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PMID:Complications of low-dose heparin prophylaxis in gynecologic oncology surgery. 649 60

The selective antimetastatic agents p-(3,3-dimethyl-1-triazeno)benzoic acid potassium salt (DM-COOK), 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) and (+/-)1,2-di(3,5-dioxopiperazin-1-yl)propane (ICRF-159) have been shown to markedly depress the formation of spontaneous hematogenous metastases in mice bearing s.c. Lewis lung carcinoma, with a mechanism unrelated to cytotoxicity for tumor cells. The effects on hemostasis of DM-COOK, DTIC and ICRF-159 have thus been examined in comparison with those of a purely cytotoxic agent, cyclophosphamide, in mice bearing i.m. Lewis lung carcinoma. The parameters considered are the number of platelets and their aggregability, prothrombin and partial thromboplastin times, plasma fibrinogen concentration and tumor cell procoagulant activity. Slight variations are caused by drug treatment in tumor-bearing mice as compared with untreated tumor-bearing controls; the pattern of effects of the selective antimetastatic agents does not differ from that of the reference cytotoxic compound used, cyclophosphamide. These data thus indicate that the effects on hemostasis of the drugs examined can contribute only marginally to their antimetastatic action, since more pronounced effects on hemostasis have been shown to be required to significantly affect metastasis formation.
Eur J Cancer Clin Oncol 1984 Jul
PMID:Hemostasis and mechanism of action of selective antimetastatic drugs in mice bearing Lewis lung carcinoma. 654 Jan 95

The effect of ketoprofen (Orudis, Farmitalia) on ADP, epinephrine (EPI) and collagen (COLL) induced platelet aggregation (PlA), simplate bleeding time (SBT), partial thromboplastin time (PTT) and per cent prothrombin activity (PrA) was studied in eleven patients, four males and seven females (median age 59 years) with rheumatoid arthritis (six cases), cancer (four cases) and osteoarthrosis (one case). Tests were performed before and 1, 8 and 24 hours after a single intravenous dose (600 mg) of ketoprofen and on Days 4 and 8 during a 7-day treatment (200 mg i.v. every 8 hours) and 1 day after withdrawal of the drug. PTT and PrA were not affected by the drug. Bleeding time was not significantly modified by the acute treatment, but was prolonged during the subacute course, though it was not different from baseline values at the end of the trial. Significant reduction of platelet aggregation was seen in both acute and subacute conditions with complete or almost complete recovery 36 hours after the last dose. It is concluded that ketoprofen affects platelets with readily reversible inhibition of in vitro aggregation and a slight increase of bleeding time.
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PMID:Effects of intravenous high doses of ketoprofen on blood clotting, bleeding time and platelet aggregation in man. 661 83


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