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G Hienert

Publications and source records attributed to G Hienert.

21 records · Page 2Linked to original sources

Increased urokinase activity to antigen ratio in human renal-cell carcinoma.

Eighteen patients with renal-cell carcinoma have been investigated in an attempt to elucidate the ratio of active urokinase enzyme to urokinase antigen in the tumor and adjacent normal kidney. The tumor itself exhibited a significantly increased total fibrinolytic activity, an increase in the relative contribution of anti-urokinase IgG-inhibitable plasminogen activator activity and increased levels of urokinase antigen when compared to normal renal tissue. In tumor-adjacent tissue total fibrinolytic activity was also, but not significantly, increased, this increase being completely due to tissue-type plasminogen activator. Correlation of active urokinase-type plasminogen activator with urokinase antigen revealed that in tumor tissue the enzyme was present to more than 70% in its active form whereas in tumor-adjacent tissue and normal renal tissue only half of the enzyme appeared to be active. No correlation was obtained between urokinase antigen present in one of the 3 tissues investigated and plasma urokinase antigen.

Adult↗

Plasminogen activator activity in bone metastases of prostatic carcinomas as compared to primary tumors.

The plasminogen activator content of extracts of 14 prostatic carcinomas and the respective bone metastases was determined and found to be at an average 1.5 times higher in the extracts from bone metastases than in the primary tumors. Furthermore, the relative contribution of the two known types of plasminogen activators, urokinase-type (u-PA) and tissue-type (t-PA), was evaluated using specific antibodies. About 70% of the plasminogen activator activity in the primary tumors was inhibited by anti-urokinase IgG, whereas the same antibody nearly completely inhibited the plasminogen activator activity in extracts from bone metastases. Using antibodies against t-PA about 30% of the plasminogen activator activity could be quenched in extracts of primary tumors but less than 10% in extracts of bone metastases. Further studies revealed that the increased amount of u-PA in extracts of bone metastases is not caused by different extractability but is also reflected by a relative increase in the amount of u-PA demonstrable by immune histochemical techniques using anti-urokinase IgG. Upon purification, the predominant plasminogen activator from extracts of bone metastases could also be identified physicochemically as urokinase.

Adenocarcinoma↗

[Tissue plasminogen activator activity in early prostatic cancer and in bone metastases of prostatic cancer].

Most malignant cells exhibit increased plasminogen activator activity which, in turn, leads to the formation of the fibrinolytically active enzyme, plasmin. Since solid tumours in man are surrounded by a fibrin network, the fibrinolytic activity of the tumour may influence tumour growth and metastasis. In the present study plasminogen activator activity, as assessed in purified extracts, was compared in benign hyperplasia of the prostate (group A, n = 6), non-metastasizing+ prostatic carcinoma (group B, n = 26), and in prostatic carcinoma with bone metastasis (group C, n = 10). Plasminogen activator activity was significantly higher in prostatic carcinoma than in hyperplasia, but there was no significant difference in plasminogen activator activity between prostate carcinoma with or without bone metastasis. However, plasminogen activator activity in the bone metastasis cells was significantly higher than in the primary tumour. If a positive correlation between fibrinolytic activity of the tumour and the metastasizing capacity were postulated, particular importance could be attached to bone metastasis in prostatic cancer.

Bone Neoplasms↗