Analysis of fibrinolytic proteins in relation to DNA ploidy in prostate cancer

The tissue concentrations of urokinase‐type plasminogen activator (u‐PA), urokinase‐type plasminogen activator receptor (u‐PAR), plasminogen activator inhibitor type 1 (PAI‐1) and tissue‐type plasminogen activator (t‐PA) were investigated by an ELISA technique in normal and malignant samples of the...

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Veröffentlicht in:International journal of cancer 1998-10, Vol.78 (3), p.320-325
Hauptverfasser: Plas, Eugen, Carroll, Veronica A., Jilch, Ruth, Mihaly, Judith, Vesely, Michael, Ulrich, Walter, Pflüger, Heinz, Binder, Bernd R.
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Sprache:eng
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Zusammenfassung:The tissue concentrations of urokinase‐type plasminogen activator (u‐PA), urokinase‐type plasminogen activator receptor (u‐PAR), plasminogen activator inhibitor type 1 (PAI‐1) and tissue‐type plasminogen activator (t‐PA) were investigated by an ELISA technique in normal and malignant samples of the prostate from 24 patients undergoing radical prostatectomy for organ‐confined prostate cancer. The median concentration of u‐PA was significantly higher in cancerous than in normal prostate tissue (p = 0.006). No significant increase of u‐PAR, PAI‐1 and t‐PA was found in cancer tissue in comparison with the benign samples (p > 0.05). Assessment of the relationship between fibrinolytic proteins and DNA ploidy revealed an increased u‐PA, u‐PAR and PAI‐1 in diploid prostate cancer as compared with the normal controls. However, in aneuploid cancer u‐PA remained high but u‐PAR and PAI‐1 were decreased. This led to a higher local concentration of u‐PA in aneuploid samples than in normal prostate and in diploid prostate cancer. No alteration of median t‐PA was found in benign prostate or in diploid or aneuploid prostate cancer. The altered expression of u‐PA, u‐PAR and PAI‐1 in diploid and aneuploid prostate cancer suggests a possible role of fibrinolytic proteins in the different biologic behavior of tumors, and may be one explanation for the higher metastatic potential of aneuploid tumors. Int. J. Cancer 78:320–325, 1998© 1998 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/(SICI)1097-0215(19981029)78:3<320::AID-IJC11>3.0.CO;2-A