Fibrinolysis, thromboplastin activity and localization of radioiodinated fibrinogen in experimental tumors

Hilgard, P.; Hiemeyer, V.

doi:10.1016/0014-2964(70)90015-0

Cited by 10 publications

(4 citation statements)

References 7 publications

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“…Thromboplastin activity of cancers does indeed correlate well with their localized uptake of fibrinogen in vivo (Hilgard and Hiemeyer, 1970). Fibrin formed apparently following thromboplastin action has also previously been shown to surround cancer metastases and their individual cells and to occur extravascularly (Zacharski et al, 1983) as well as in vessels.…”

Section: Discussionmentioning

confidence: 73%

Thromboplastin release, but not content, correlates with spontaneous metastasis of cancer cells

Girimstad

Prydz

1988

Intl Journal of Cancer

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No previous studies on the possible contribution of cancer-cell procoagulants to metastasis have fulfilled all the criteria for attaining biologically relevant and readily interpretable data (Grimstad et al., 1986), viz: (1) Spontaneous metastasis from primary tumors should be assessed in syngeneic animals; (2) cloned cell lines should be used to correlate cell properties, because heterogeneity within the cell lines employed is a source of serious error; (3) enough clones, derived from the same original tumor, should be used to identify only nonrandom correlations. Observing these criteria, we examined the procoagulant activities of 19 murine fibrosarcoma cell clones and 4 uncloned cell lines with high to moderate or low potential for lung metastases formation. The procoagulant activity found was exclusively of the thromboplastin (tissue factor, factor III) type. It occurred in all cell homogenates, but the quantities did not correlate with metastatic potential. In contrast, all highly to moderately metastatic cell clones and lines from 2 different fibrosarcomas shed thromboplastin activity into the culture medium, whereas no weakly metastatic cells did. Histological examination further supported these indications that release of thromboplastin from cancer cells can promote metastasis by initiating blood clotting and thereby facilitating arrest of the cancer cells in target organ vessels. Examination of a third fibrosarcoma showed that release of thromboplastin activity is not necessary for metastasis in all tumors.

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Section: Discussionmentioning

confidence: 73%

Thromboplastin release, but not content, correlates with spontaneous metastasis of cancer cells

Girimstad

Prydz

1988

Intl Journal of Cancer

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“…The lack of evidence for microclots at necropsy in patients with tumour cell emboli may be due to a spontaneous fibrinolysis between death and tissue fixation and only in very favourable conditions may they be observed (Bull & Kuhn, 1970;Cohan et al, 1972). A marked decrease of the fibrinolytic potential has been reported in patients with disseminated carcinoma (Thornes, 1967;Soong & Miller, 1970) and in autochthonous experimental tumours (Hilgard & Hiemeyer, 1970). It seems likely that the development of microangiopathic haemolytic anaemia in patients with tumour cell emboli is the coincidence of a variety of factors, producing an imbalance between fibrin formation and fibrinolysis which allows the persistence of intravascular microclots.…”

Section: Discussionmentioning

confidence: 95%

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Hilgard

Gordon‐Smith

1974

Br J Haematol

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Summary. The mechanism by which disseminated carcinoma may induce microangiopathic haemolytic anaemia has been studied in rats using intravenous injections of Walker carcinosarcoma‐256 cells. Following the injection of tumour cells there was sequestration of radio‐labelled fibrinogen and platelets in the lungs and a simultaneous fall in peripheral platelet count and rise in free plasma haemoglobin. Anti‐fibrinolytic treatment (EACA) and triamcinolone accentuated the changes whereas heparin abolished the effect. Electron microscopy demonstrated fibrin and platelet deposition around tumour cells. It is concluded that intravascular coagulation around tumour cell emboli is an important mechanism in the production of microangiopathic haemolytic anaemia in disseminated carcinoma.

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“…The methods described recently have been applied to different experimental conditions and significant and reproducible results were obtained [6,7]. Obviously, the rat is suitable to study the activation of fibrinolysis under physiological and pathological conditions in animals.…”

Section: Discussionmentioning

confidence: 99%

Comparative Studies of the Fibrinolytic System in Rats and Humans

Hilgard¹

1972

Pathophysiol Haemos Thromb

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Components of the fibrinolytic system were determined in human and rat plasma. Rat plasma has a significantly higher plasminogen activator content which is counterbalanced by a higher plasmin inhibitor level. The plasma plasminogen concentration is somewhat higher in humans. The trypsin inhibitor did not differ significantly in humans and rats. Identical values for plasminogen were found in human plasma when activated with streptokinase or urokinase. The necessity of a correct streptokinase concentration in the assay system is stressed. From the data presented it is concluded that the rat is a suitable animal to study fibrinolysis under experimental conditions.

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Fibrinolysis, thromboplastin activity and localization of radioiodinated fibrinogen in experimental tumors

Cited by 10 publications

References 7 publications

Thromboplastin release, but not content, correlates with spontaneous metastasis of cancer cells

Thromboplastin release, but not content, correlates with spontaneous metastasis of cancer cells

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Comparative Studies of the Fibrinolytic System in Rats and Humans

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