Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor
The presence of metastases in regional lymph nodes is a strong indicator of poor patient survival in many types of cancer. It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2005-08, Vol.65 (15), p.6901-6909 |
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| creator | JIANMIN LIN LALANI, Alshad S MITALO, Kari JOOSS, Karin HARDING, Thomas C GONZALEZ, Melissa WU, Wei-Wei BO LUAN GUANG HUAN TU KOPRIVNIKAR, Kathryn VANROEY, Melinda J YULONG HE |
| description | The presence of metastases in regional lymph nodes is a strong indicator of poor patient survival in many types of cancer. It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal role in the promotion of metastasis to regional lymph nodes. In this study, human prostate and melanoma tumor models that preferentially metastasize to the lymph nodes following s.c. tumor cell implantation were established from lymph node metastases via in vivo selection. Melanoma tumor cell sublines established from lymph node metastasis express higher amounts of VEGF-C than the parental tumor cells. The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation. In addition, sVEGFR3-Fc serum levels required for efficient blockade of lymph node metastases are strictly dependent on the VEGF-C levels generated by the primary tumor. Recombinant adeno-associated virus-mediated gene transfer of sVEGFR3-Fc may represent a feasible therapeutic strategy for blockade of lymphogenous metastasis. |
| doi_str_mv | 10.1158/0008-5472.CAN-05-0408 |
| format | Article |
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It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal role in the promotion of metastasis to regional lymph nodes. In this study, human prostate and melanoma tumor models that preferentially metastasize to the lymph nodes following s.c. tumor cell implantation were established from lymph node metastases via in vivo selection. Melanoma tumor cell sublines established from lymph node metastasis express higher amounts of VEGF-C than the parental tumor cells. The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation. In addition, sVEGFR3-Fc serum levels required for efficient blockade of lymph node metastases are strictly dependent on the VEGF-C levels generated by the primary tumor. Recombinant adeno-associated virus-mediated gene transfer of sVEGFR3-Fc may represent a feasible therapeutic strategy for blockade of lymphogenous metastasis.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-05-0408</identifier><identifier>PMID: 16061674</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenoviridae - genetics ; Animals ; Antineoplastic agents ; Biological and medical sciences ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - pathology ; Carcinoma, Renal Cell - therapy ; Cell Line, Tumor ; Female ; Gene Transfer Techniques ; Genetic Therapy - methods ; Genetic Vectors - genetics ; Humans ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Kidney Neoplasms - therapy ; Lung Neoplasms - secondary ; Lymphatic Metastasis ; Male ; Medical sciences ; Melanoma - genetics ; Melanoma - pathology ; Melanoma - therapy ; Mice ; Mice, Nude ; Neoplasms - genetics ; Neoplasms - pathology ; Neoplasms - therapy ; Pharmacology. Drug treatments ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms - therapy ; Tumors ; Vascular Endothelial Growth Factor Receptor-3 - biosynthesis ; Vascular Endothelial Growth Factor Receptor-3 - blood ; Vascular Endothelial Growth Factor Receptor-3 - genetics</subject><ispartof>Cancer research (Chicago, Ill.), 2005-08, Vol.65 (15), p.6901-6909</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c619t-f576e708c5ba650a3b159554711884a213903d521aa4a72bab00b0453a7482943</citedby><cites>FETCH-LOGICAL-c619t-f576e708c5ba650a3b159554711884a213903d521aa4a72bab00b0453a7482943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16988971$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16061674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JIANMIN LIN</creatorcontrib><creatorcontrib>LALANI, Alshad S</creatorcontrib><creatorcontrib>MITALO, Kari</creatorcontrib><creatorcontrib>JOOSS, Karin</creatorcontrib><creatorcontrib>HARDING, Thomas C</creatorcontrib><creatorcontrib>GONZALEZ, Melissa</creatorcontrib><creatorcontrib>WU, Wei-Wei</creatorcontrib><creatorcontrib>BO LUAN</creatorcontrib><creatorcontrib>GUANG HUAN TU</creatorcontrib><creatorcontrib>KOPRIVNIKAR, Kathryn</creatorcontrib><creatorcontrib>VANROEY, Melinda J</creatorcontrib><creatorcontrib>YULONG HE</creatorcontrib><title>Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>The presence of metastases in regional lymph nodes is a strong indicator of poor patient survival in many types of cancer. It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal role in the promotion of metastasis to regional lymph nodes. In this study, human prostate and melanoma tumor models that preferentially metastasize to the lymph nodes following s.c. tumor cell implantation were established from lymph node metastases via in vivo selection. Melanoma tumor cell sublines established from lymph node metastasis express higher amounts of VEGF-C than the parental tumor cells. The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation. In addition, sVEGFR3-Fc serum levels required for efficient blockade of lymph node metastases are strictly dependent on the VEGF-C levels generated by the primary tumor. Recombinant adeno-associated virus-mediated gene transfer of sVEGFR3-Fc may represent a feasible therapeutic strategy for blockade of lymphogenous metastasis.</description><subject>Adenoviridae - genetics</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Carcinoma, Renal Cell - therapy</subject><subject>Cell Line, Tumor</subject><subject>Female</subject><subject>Gene Transfer Techniques</subject><subject>Genetic Therapy - methods</subject><subject>Genetic Vectors - genetics</subject><subject>Humans</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidney Neoplasms - therapy</subject><subject>Lung Neoplasms - secondary</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Melanoma - genetics</subject><subject>Melanoma - pathology</subject><subject>Melanoma - therapy</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms - therapy</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Prostatic Neoplasms - therapy</subject><subject>Tumors</subject><subject>Vascular Endothelial Growth Factor Receptor-3 - biosynthesis</subject><subject>Vascular Endothelial Growth Factor Receptor-3 - blood</subject><subject>Vascular Endothelial Growth Factor Receptor-3 - genetics</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9r3DAQxUVpaTZpP0KLLs1NqWRJlnwMS_5BaKEkvYqxLCcqtrXV2IU99LtHZpe2t8LAMOj3Rsx7hHwQ_EIIbT9zzi3TylQX28svjGvGFbevyEZoaZlRSr8mmz_MCTlF_FFGLbh-S05EzWtRG7Uhv--m59jGOaaJpp4O-3H3nJ7ClBakY5gBS0WkC8bpiUJXHhggJh9hDh39FfOCbAzdYSy6QOcME_Yhr-uAYhqWdgj0-9XN9TcmaRd82tMcfNjNKb8jb3oYMLw_9jPyeH31sL1l919v7raX98zXoplZr00dDLdet1BrDrIVutHlMCGsVVAJ2XDZ6UoAKDBVCy3nLVdaglG2apQ8I-eHvbucfi4BZzdG9GEYYArlUldbJZtaVv8FRdNIo7gpoD6APifEHHq3y3GEvHeCuzUgt5rvVvNdCchx7daAiu7j8YOlLb79VR0TKcCnIwDoYeiLmz7iP1xjbWOEfAE7WpkR</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>JIANMIN LIN</creator><creator>LALANI, Alshad S</creator><creator>MITALO, Kari</creator><creator>JOOSS, Karin</creator><creator>HARDING, Thomas C</creator><creator>GONZALEZ, Melissa</creator><creator>WU, Wei-Wei</creator><creator>BO LUAN</creator><creator>GUANG HUAN TU</creator><creator>KOPRIVNIKAR, Kathryn</creator><creator>VANROEY, Melinda J</creator><creator>YULONG HE</creator><general>American Association for Cancer Research</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>7QO</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050801</creationdate><title>Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor</title><author>JIANMIN LIN ; LALANI, Alshad S ; MITALO, Kari ; JOOSS, Karin ; HARDING, Thomas C ; GONZALEZ, Melissa ; WU, Wei-Wei ; BO LUAN ; GUANG HUAN TU ; KOPRIVNIKAR, Kathryn ; VANROEY, Melinda J ; YULONG HE</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c619t-f576e708c5ba650a3b159554711884a213903d521aa4a72bab00b0453a7482943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adenoviridae - genetics</topic><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Carcinoma, Renal Cell - therapy</topic><topic>Cell Line, Tumor</topic><topic>Female</topic><topic>Gene Transfer Techniques</topic><topic>Genetic Therapy - methods</topic><topic>Genetic Vectors - genetics</topic><topic>Humans</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Kidney Neoplasms - therapy</topic><topic>Lung Neoplasms - secondary</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Melanoma - genetics</topic><topic>Melanoma - pathology</topic><topic>Melanoma - therapy</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms - therapy</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Prostatic Neoplasms - therapy</topic><topic>Tumors</topic><topic>Vascular Endothelial Growth Factor Receptor-3 - biosynthesis</topic><topic>Vascular Endothelial Growth Factor Receptor-3 - blood</topic><topic>Vascular Endothelial Growth Factor Receptor-3 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JIANMIN LIN</creatorcontrib><creatorcontrib>LALANI, Alshad S</creatorcontrib><creatorcontrib>MITALO, Kari</creatorcontrib><creatorcontrib>JOOSS, Karin</creatorcontrib><creatorcontrib>HARDING, Thomas C</creatorcontrib><creatorcontrib>GONZALEZ, Melissa</creatorcontrib><creatorcontrib>WU, Wei-Wei</creatorcontrib><creatorcontrib>BO LUAN</creatorcontrib><creatorcontrib>GUANG HUAN TU</creatorcontrib><creatorcontrib>KOPRIVNIKAR, Kathryn</creatorcontrib><creatorcontrib>VANROEY, Melinda J</creatorcontrib><creatorcontrib>YULONG HE</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>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JIANMIN LIN</au><au>LALANI, Alshad S</au><au>MITALO, Kari</au><au>JOOSS, Karin</au><au>HARDING, Thomas C</au><au>GONZALEZ, Melissa</au><au>WU, Wei-Wei</au><au>BO LUAN</au><au>GUANG HUAN TU</au><au>KOPRIVNIKAR, Kathryn</au><au>VANROEY, Melinda J</au><au>YULONG HE</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>65</volume><issue>15</issue><spage>6901</spage><epage>6909</epage><pages>6901-6909</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>The presence of metastases in regional lymph nodes is a strong indicator of poor patient survival in many types of cancer. It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal role in the promotion of metastasis to regional lymph nodes. In this study, human prostate and melanoma tumor models that preferentially metastasize to the lymph nodes following s.c. tumor cell implantation were established from lymph node metastases via in vivo selection. Melanoma tumor cell sublines established from lymph node metastasis express higher amounts of VEGF-C than the parental tumor cells. The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation. In addition, sVEGFR3-Fc serum levels required for efficient blockade of lymph node metastases are strictly dependent on the VEGF-C levels generated by the primary tumor. Recombinant adeno-associated virus-mediated gene transfer of sVEGFR3-Fc may represent a feasible therapeutic strategy for blockade of lymphogenous metastasis.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>16061674</pmid><doi>10.1158/0008-5472.CAN-05-0408</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 2005-08, Vol.65 (15), p.6901-6909 |
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| subjects | Adenoviridae - genetics Animals Antineoplastic agents Biological and medical sciences Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - pathology Carcinoma, Renal Cell - therapy Cell Line, Tumor Female Gene Transfer Techniques Genetic Therapy - methods Genetic Vectors - genetics Humans Kidney Neoplasms - genetics Kidney Neoplasms - pathology Kidney Neoplasms - therapy Lung Neoplasms - secondary Lymphatic Metastasis Male Medical sciences Melanoma - genetics Melanoma - pathology Melanoma - therapy Mice Mice, Nude Neoplasms - genetics Neoplasms - pathology Neoplasms - therapy Pharmacology. Drug treatments Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology Prostatic Neoplasms - therapy Tumors Vascular Endothelial Growth Factor Receptor-3 - biosynthesis Vascular Endothelial Growth Factor Receptor-3 - blood Vascular Endothelial Growth Factor Receptor-3 - genetics |
| title | Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor |
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