Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation activity in the blood of rats during the development of Guerin epithelioma was studied. Clotting time, level of fibrinogen and some coagulation factors (II, V, VII + X) in the plasma were determined and thromboelastographic studies were performed. Two periods of blood hypercoagulability were observed in the process of epithelioma development. The first a short-term period, was noticed during the first days following the implantation of the neoplastic tissue. The second took place during the intensive growth of the primary tumor and metastases.
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PMID:Blood coagulation changes in rats during development of epithelioma. 271 22

Patients with malignant tumors of the upper respiratory tract showed higher concentrations of fibrinogen in plasma the level of which was correlated with the stage of disease. Measurements of the protein in the course of radiation therapy demonstrated that two months after effective treatment fibrinogen concentrations decreased to normal values and remained at that level throughout the remission time. If radiation therapy was ineffective, fibrinogen concentrations remained high during 2 to 4 months after exposure. Metastases and recurrent tumors caused a drastic increase in the fibrinogen content, the change occasionally occurring prior to clinical manifestations. In view of this, plasma fibrinogen can be recommended as an additional measure that can be used to evaluate therapy effectiveness, to prognose the course of disease and to identify metastases in patients with malignant tumors of the upper respiratory tract.
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PMID:[Analysis of plasma fibrinogen in evaluating the effectiveness and prognosis of polyradiomodifying therapy of malignant tumors of the upper respiratory tract]. 272 81

The mechanism by which the murine fibrosarcoma clone PAK 17.15 induces platelet aggregation [tumor cell-induced platelet aggregation (TCIPA)] was studied because platelet activation by this clone is necessary for metastasis to the lungs. PAK 17.15 TCIPA was completely inhibited by ADP-clearing enzymes, such as apyrase, or a mixture of creatine phosphate and creatine phosphokinase. Thrombin and collagen were not involved in PAK 17.15 TCIPA. Further studies showed that ADP is most likely secreted from activated platelets and that membrane protein(s) on PAK 17.15 cells are responsible for platelet activation. Inasmuch as ADP-dependent platelet aggregation requires fibrinogen and can be inhibited by the Gly-Arg-Gly-Asp-Ser (GRGDS) synthetic peptide, the effect of this peptide on PAK 17.15 TCIPA was studied. PAK 17.15 TCIPA was completely inhibited by the GRGDS peptide (0.4 mM) but not by a control peptide, Gly-Arg-Gly-Glu-Ser (0.8 mM). In addition, the GRGDS peptide inhibited adhesion of PAK 17.15 cells to immobilized fibronectin. As expected, the GRGDS peptide almost completely inhibited lung colonization by iv injected PAK 17.15 cells in C57BL/6 mice. Our results indicate that GRGDS may inhibit pulmonary metastases by interfering with TCIPA as well as with tumor cell adhesion to extra-cellular matrix components in the host.
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PMID:Inhibition of tumor cell-induced platelet aggregation and experimental tumor metastasis by the synthetic Gly-Arg-Gly-Asp-Ser peptide. 318 95

The increased risk of thrombosis seen in patients with malignancy also was recently confirmed in breast cancer patients undergoing hormonal or chemotherapeutic treatment. Besides changes within the coagulation system, alterations of hemorheologic variables have been implicated in the genesis of thrombosis. We evaluated plasma viscosity, erythrocyte aggregation, fibrinogen level, sedimentation rate, hematocrit concentration, and protein concentration in patients with breast cancer at the time of primary diagnosis and during follow-up with or without treatment. We then compared the results to a control group without malignant or infectious disease. Plasma viscosity and erythrocyte aggregation were significantly higher in patients with malignant disease, with a further increase at the time of dissemination. Plasma fibrinogen level was significantly higher only at the time of dissemination. The influence of therapy on hemorheologic variables was minor. Tumor volume was the most important factor. As individual values vary considerably and form a continuous spectrum, no cutoff line between normal and pathologic values can be defined. However, high values should induce further measures to diagnose metastatic disease. Second, these factors could explain the relative inefficiency of thrombosis prophylaxis in this patient group and suggest the addition of rheologically active drugs to the treatment regimen.
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PMID:Hemorheologic variables in breast cancer patients at the time of diagnosis and during treatment. 338 35

This study reports an unusual subpopulation of rats bearing transplanted tumors approximately 50% of the total and apparently unrelated to the presence of metastases, that exhibited shortened bleeding times despite reduced platelet numbers and/or fibrinogen levels. The remaining rats exhibited the expected inverse relationships between bleeding time and platelet numbers and/or fibrinogen level. Tumors were hepatomas and squamous cell carcinomas initially induced in the Fischer strain of rats and carried by passage through tissue culture or syngenic recipient animals.
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PMID:Blood coagulation abnormalities in Fischer strain rats bearing tumors. 360 Jan 66

Platelet function following inoculation of chemically induced carcinoma was evaluated in the rat. The original line of tumor (NGW1) was obtained using N-methyl-N-nitrosoguanidine. After trypsin homogenation a cell suspension of 0.3 X 10(6) viable tumor cells was injected subserosally in the cecum of each animal. Controls received injections of equal volumes of 0.9% NaCl solution or trypsin. The animals were subjected to laparotomy 2, 4, and 6 weeks after inoculation. Platelet function was assessed in vivo by measuring bleeding time and blood loss during mesenteric vessel transection or liver resection upon laparotomy. Hemoglobin, hematocrit, platelet count, activated partial thromboplastin time, platelet aggregation, thromboxane B2, platelet factor 4, and fibrinogen levels were evaluated after sacrifice by exsanguination. Significant decrease in bleeding time and blood loss was observed in animals with local primary tumors as well as in rats with lymph node metastases. Hemoglobin and hematocrit were decreased in the presence of metastases. Platelet count was not changed. Activated partial thromboplastin time was not affected by the presence of tumor. Platelet aggregation in vitro was accelerated in the presence of primary tumor or lymph node metastases, as well as following addition of tumor cells to platelet suspensions. No changes in thromboxane B2 or platelet factor 4 could be registered. Fibrinogen levels were decreased in the presence of liver metastases. Enhancement of primary hemostasis and platelet function in the presence of colon carcinoma in the rat was demonstrated both in vivo and in vitro. Direct or indirect interaction of the tumor cell with thrombocytes may play a role in determining the metastatic potential of the neoplasm.
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PMID:Hemostasis following inoculation and during spreading of colon carcinoma in the rat. 375 13

The effect of anticoagulant drugs on formation of experimental tumor metastases after i.v. inoculation of BL6 melanoma or Lewis lung carcinoma (3LL) cells was studied in mice with stimulated or depressed natural killer (NK) cell activity. When mice were treated with anticoagulants (warfarin or heparin) or when NK cell activity was stimulated by polyinosinic-polycytidylic acid, significant antimetastatic effects were observed; these effects were substantially augmented when the treatments were combined. However, when NK reactivity of mice was suppressed by anti-asialo GM1 serum or cyclophosphamide, the antimetastatic effects of warfarin and heparin were diminished or completely abrogated. In some experiments, the anticoagulants had a partial effect in mice treated with cyclophosphamide or anti-asialo GM1 serum and reduced at least to control levels the number of metastases in these mice. This limited antimetastatic effect of the anticoagulants was mostly due to the action of residual NK cells, since it was completely abrogated in mice whose NK cell activity was more completely suppressed by two injections of anti-asialo GM1 serum. In addition, the low NK reactivity of 3-week-old C57BL/6 or beige mice was sufficient to support the antimetastatic effects of the anticoagulants, effects that completely disappeared after these mice were treated with anti-asialo GM1 serum. Augmentation or abrogation of the antimetastatic effects of heparin after polyinosinic-polycytidylic acid or anti-asialo GM1 treatments, respectively, was observed in athymic nude and allogeneic BALB/c mice that received i.v. injections of B16F1 melanoma cells, indicating that the antimetastatic effects of anticoagulants depend on the presence of active NK rather than T-cells. Furthermore, adoptive transfer of NK-competent but not NK-depleted syngeneic spleen cells restored the antimetastatic effect of heparin in cyclophosphamide-treated mice. Warfarin treatment increased the elimination of radiolabeled BL6 melanoma cells from the lungs of normal mice, and the rate of tumor cell elimination was further potentiated when NK cell activity was stimulated by polyinosinic-polycytidylic acid. In contrast, after anti-asialo GM1 treatment, warfarin had no effect on the survival of i.v. administered tumor cells. Covering of YAC-1 or 3LL tumor cells with fibrin after in vitro exposure with fibrinogen and thrombin substantially protected them from the in vitro cytotoxic action of NK or lymphokine-activated killer cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Augmentation of the antimetastatic effect of anticoagulant drugs by immunostimulation in mice. 380 83

X-irradiation administered to nude mice and the ensuing pulmonary metastasis of injected human tumor cells were investigated. When human tumor cells (5 X 10(5)) were injected into the tail vein of male adult nude mice 5 days after 3 Gy whole-body X-irradiation, the incidence of pulmonary metastasis was more frequent in the irradiated mice than in the nonirradiated controls. Platelet aggregation and fibrin deposition around the tumor cells were present in the capillaries of the lung in the irradiated mice while prominent neutrophilic infiltration was noted around the tumor cells in the nonirradiated controls. Fibrinolytic activity of the lung was decreased in the irradiated mice, while serum fibrinogen level was increased after irradiation. Natural killer cell activity was decreased after irradiation. We conclude from this study that increase in serum fibrinogen levels and decrease in fibrinolytic activity of the lung, as a target organ, together with decreased infiltration of neutrophils, may be related to the trapping and lodgement of tumor cells when nude mice are subjected to irradiation.
Invasion Metastasis 1985
PMID:Fate of intravenously injected human tumor cells in the lung of nude mice following whole-body X-irradiation. 388 35

Acquired dysfibrinogenemia has not been previously reported as a paraneoplastic marker for malignancy. This report describes the clinical course of a patient who at the time of diagnosis of nonmetastatic renal cell carcinoma had dysfibrinogenemia characterized by prolongation of the thrombin and Reptilase times and increased sialic acid content of the purified fibrinogen. The thrombin and Reptilase times returned toward normal values after nephrectomy but became abnormal with the development of nonhepatic metastases. It is concluded that acquired dysfibrinogenemia can be part of a paraneoplastic syndrome and is a sensitive plasma marker for tumor progression.
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PMID:Acquired dysfibrinogenemia. Paraneoplastic syndrome in renal cell carcinoma. 398 42

Hepatic resection for metastatic colorectal cancer has been reported in over 700 patients. However, approximately 5000 patients each year are candidates for surgical excision. Since 1972, 25 patients have undergone hepatic resection for colorectal metastases at New York University. Potentially curable synchronous lesions were detected by preoperative liver chemistries and operative palpation. Patients were screened for metachronous lesions by serial liver chemistries and carcinoembryonic antigen (CEA) determinations; when clinical findings or laboratory findings were either positive or equivocal, then scanning techniques were used. Most patients had solitary lesions (20). Thirteen of 25 lesions were synchronous; 12 were metachronous. Anatomic lobectomy was performed in 13 patients (6 extended resections); and wedge resection was performed in 12. The operative mortality rate was four per cent; the 2-year survival rate, 65%; the 5-year survival rate, 25%. Hypertonic dextrose solutions were administered during and after operation. Post-operative albumin requirements ranged from 200 to 300 grams/day. Coagulation factors II, V, VII, and fibrinogen decreased after surgery to 30 to 50% of their preoperative levels. Subsequent elevation of these factors correlated with increased bile production and improvement in liver chemistries 10 to 14 days after operation. At present, hepatic resection for colorectal metastases provides the only potential method of salvage, offering a 20 to 25% long-term survival rate.
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PMID:Hepatic resection for metastatic colon and rectal cancer. An evaluation of preoperative and postoperative factors. 401 24


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