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 |
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| container_title | International journal of cancer |
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| creator | Plas, Eugen Carroll, Veronica A. Jilch, Ruth Mihaly, Judith Vesely, Michael Ulrich, Walter Pflüger, Heinz Binder, Bernd R. |
| description | 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. |
| doi_str_mv | 10.1002/(SICI)1097-0215(19981029)78:3<320::AID-IJC11>3.0.CO;2-A |
| format | Article |
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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.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/(SICI)1097-0215(19981029)78:3<320::AID-IJC11>3.0.CO;2-A</identifier><identifier>PMID: 9766566</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aged ; Biological and medical sciences ; DNA - genetics ; DNA, Neoplasm - genetics ; Enzyme-Linked Immunosorbent Assay ; Fibrinolysis ; Humans ; Immunohistochemistry ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Plasminogen Activator Inhibitor 1 - analysis ; Ploidies ; Prostate - chemistry ; Prostate - metabolism ; Prostatic Neoplasms - chemistry ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Receptors, Cell Surface - analysis ; Receptors, Urokinase Plasminogen Activator ; Tissue Plasminogen Activator - analysis ; Tumors of the urinary system ; Urinary tract. 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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.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>DNA - genetics</subject><subject>DNA, Neoplasm - genetics</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fibrinolysis</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Plasminogen Activator Inhibitor 1 - analysis</subject><subject>Ploidies</subject><subject>Prostate - chemistry</subject><subject>Prostate - metabolism</subject><subject>Prostatic Neoplasms - chemistry</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, Cell Surface - analysis</subject><subject>Receptors, Urokinase Plasminogen Activator</subject><subject>Tissue Plasminogen Activator - analysis</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><subject>Urokinase-Type Plasminogen Activator - analysis</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE2P0zAQhi0EWsrCT0DKAaHdQ8pMnNhxQaAoy0fRansABLeR49qSUZqUOBXKv8ehpReQOFmaefzOq4exNwhLBMheXH1a1-trBCVTyLC4QqVKhExdy3LFX_EMVqtqfZOuP9aIr_kSlvXmZZZW99ji_Oc-W8QkSCVy8ZA9CuE7AGIB-QW7UFKIQogFu6s63U7Bh6R3ifPN4Lu-nUZvkv3Qj9Z3IfFdMthWj77vkrFPbu6qZN_2fjvNm0iFUY82MbozdnjMHjjdBvvk9F6yL-_efq4_pLeb9-u6uk1NLgtMhQGh8yy3SmupbF42xlrVcLdFYSQKdHkButSFKzMoOaDWDZS2AZc7lILzS_b8mBvv_zjYMNLOB2PbVne2PwQSShWopIrg1yNoYtEwWEf7we_0MBECzaaJZtM0W6PZGv0xTbIkTtE0UTRNv03HAVC9oYyqmPz0VOHQ7Oz2nHtSG_fPTnsdjG7dEAX5cMayPF4r84h9O2I_fWunv9r9t9y_uh0H_BfdNqWK</recordid><startdate>19981029</startdate><enddate>19981029</enddate><creator>Plas, Eugen</creator><creator>Carroll, Veronica A.</creator><creator>Jilch, Ruth</creator><creator>Mihaly, Judith</creator><creator>Vesely, Michael</creator><creator>Ulrich, Walter</creator><creator>Pflüger, Heinz</creator><creator>Binder, Bernd R.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19981029</creationdate><title>Analysis of fibrinolytic proteins in relation to DNA ploidy in prostate cancer</title><author>Plas, Eugen ; Carroll, Veronica A. ; Jilch, Ruth ; Mihaly, Judith ; Vesely, Michael ; Ulrich, Walter ; Pflüger, Heinz ; Binder, Bernd R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4751-6c06a424e9aa79e48bcee9b3fd16c7161f450a8a5f8208301aab08eb0f4f17633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>DNA - genetics</topic><topic>DNA, Neoplasm - genetics</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fibrinolysis</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Plasminogen Activator Inhibitor 1 - analysis</topic><topic>Ploidies</topic><topic>Prostate - chemistry</topic><topic>Prostate - metabolism</topic><topic>Prostatic Neoplasms - chemistry</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Receptors, Cell Surface - analysis</topic><topic>Receptors, Urokinase Plasminogen Activator</topic><topic>Tissue Plasminogen Activator - analysis</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><topic>Urokinase-Type Plasminogen Activator - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Plas, Eugen</creatorcontrib><creatorcontrib>Carroll, Veronica A.</creatorcontrib><creatorcontrib>Jilch, Ruth</creatorcontrib><creatorcontrib>Mihaly, Judith</creatorcontrib><creatorcontrib>Vesely, Michael</creatorcontrib><creatorcontrib>Ulrich, Walter</creatorcontrib><creatorcontrib>Pflüger, Heinz</creatorcontrib><creatorcontrib>Binder, Bernd R.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plas, Eugen</au><au>Carroll, Veronica A.</au><au>Jilch, Ruth</au><au>Mihaly, Judith</au><au>Vesely, Michael</au><au>Ulrich, Walter</au><au>Pflüger, Heinz</au><au>Binder, Bernd R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of fibrinolytic proteins in relation to DNA ploidy in prostate cancer</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>1998-10-29</date><risdate>1998</risdate><volume>78</volume><issue>3</issue><spage>320</spage><epage>325</epage><pages>320-325</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>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.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>9766566</pmid><doi>10.1002/(SICI)1097-0215(19981029)78:3<320::AID-IJC11>3.0.CO;2-A</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Biological and medical sciences DNA - genetics DNA, Neoplasm - genetics Enzyme-Linked Immunosorbent Assay Fibrinolysis Humans Immunohistochemistry Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Plasminogen Activator Inhibitor 1 - analysis Ploidies Prostate - chemistry Prostate - metabolism Prostatic Neoplasms - chemistry Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Receptors, Cell Surface - analysis Receptors, Urokinase Plasminogen Activator Tissue Plasminogen Activator - analysis Tumors of the urinary system Urinary tract. Prostate gland Urokinase-Type Plasminogen Activator - analysis |
| title | Analysis of fibrinolytic proteins in relation to DNA ploidy in prostate cancer |
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