Targeting the tumor and its microenvironment by a dual-function decoy Met receptor
Met, the receptor for hepatocyte growth factor (HGF), is activated in human cancer by both ligand-dependent and -independent mechanisms. We engineered a soluble Met receptor (decoy Met) that interferes with both HGF binding to Met and Met homodimerization. By lentiviral vector technology, we achieve...
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| Veröffentlicht in: | Cancer cell 2004-07, Vol.6 (1), p.61-73 |
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| container_title | Cancer cell |
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| creator | Michieli, Paolo Mazzone, Massimiliano Basilico, Cristina Cavassa, Silvia Sottile, Antonino Naldini, Luigi Comoglio, Paolo M |
| description | Met, the receptor for hepatocyte growth factor (HGF), is activated in human cancer by both ligand-dependent and -independent mechanisms. We engineered a soluble Met receptor (decoy Met) that interferes with both HGF binding to Met and Met homodimerization. By lentiviral vector technology, we achieved local or systemic delivery of decoy Met in mice. We provide evidence that in vivo expression of decoy Met (1) inhibits tumor cell proliferation and survival in a variety of human xenografts, (2) impairs tumor angiogenesis by preventing host vessel arborization, (3) suppresses or prevents the formation of spontaneous metastases, and (4) synergizes with radiotherapy in inducing tumor regression, without (5) affecting housekeeping physiological functions in the adult animal. |
| doi_str_mv | 10.1016/j.ccr.2004.05.032 |
| format | Article |
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We engineered a soluble Met receptor (decoy Met) that interferes with both HGF binding to Met and Met homodimerization. By lentiviral vector technology, we achieved local or systemic delivery of decoy Met in mice. We provide evidence that in vivo expression of decoy Met (1) inhibits tumor cell proliferation and survival in a variety of human xenografts, (2) impairs tumor angiogenesis by preventing host vessel arborization, (3) suppresses or prevents the formation of spontaneous metastases, and (4) synergizes with radiotherapy in inducing tumor regression, without (5) affecting housekeeping physiological functions in the adult animal.</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2004.05.032</identifier><identifier>PMID: 15261142</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiogenesis Inhibitors - pharmacology ; Animals ; Dimerization ; Disease-Free Survival ; Female ; Gene Transfer Techniques ; Genetic Therapy ; Genetic Vectors ; Hepatocyte Growth Factor - genetics ; Hepatocyte Growth Factor - metabolism ; Humans ; Lentivirus - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - secondary ; Lung Neoplasms - therapy ; Mammary Neoplasms, Experimental - metabolism ; Mammary Neoplasms, Experimental - pathology ; Mammary Neoplasms, Experimental - therapy ; Mice ; Mice, Nude ; Neoplasm Invasiveness - pathology ; Neoplasm Invasiveness - prevention & control ; Neovascularization, Pathologic - prevention & control ; Proto-Oncogene Proteins c-met - genetics ; Proto-Oncogene Proteins c-met - metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays</subject><ispartof>Cancer cell, 2004-07, Vol.6 (1), p.61-73</ispartof><rights>2004 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c522t-d0cc07db1ff3ac6024e825d4e1abb577112f07670cd83ee53f46ede52fb3d7823</citedby><cites>FETCH-LOGICAL-c522t-d0cc07db1ff3ac6024e825d4e1abb577112f07670cd83ee53f46ede52fb3d7823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1535610804001448$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15261142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Michieli, Paolo</creatorcontrib><creatorcontrib>Mazzone, Massimiliano</creatorcontrib><creatorcontrib>Basilico, Cristina</creatorcontrib><creatorcontrib>Cavassa, Silvia</creatorcontrib><creatorcontrib>Sottile, Antonino</creatorcontrib><creatorcontrib>Naldini, Luigi</creatorcontrib><creatorcontrib>Comoglio, Paolo M</creatorcontrib><title>Targeting the tumor and its microenvironment by a dual-function decoy Met receptor</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>Met, the receptor for hepatocyte growth factor (HGF), is activated in human cancer by both ligand-dependent and -independent mechanisms. We engineered a soluble Met receptor (decoy Met) that interferes with both HGF binding to Met and Met homodimerization. By lentiviral vector technology, we achieved local or systemic delivery of decoy Met in mice. We provide evidence that in vivo expression of decoy Met (1) inhibits tumor cell proliferation and survival in a variety of human xenografts, (2) impairs tumor angiogenesis by preventing host vessel arborization, (3) suppresses or prevents the formation of spontaneous metastases, and (4) synergizes with radiotherapy in inducing tumor regression, without (5) affecting housekeeping physiological functions in the adult animal.</description><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Dimerization</subject><subject>Disease-Free Survival</subject><subject>Female</subject><subject>Gene Transfer Techniques</subject><subject>Genetic Therapy</subject><subject>Genetic Vectors</subject><subject>Hepatocyte Growth Factor - genetics</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>Humans</subject><subject>Lentivirus - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - secondary</subject><subject>Lung Neoplasms - therapy</subject><subject>Mammary Neoplasms, Experimental - metabolism</subject><subject>Mammary Neoplasms, Experimental - pathology</subject><subject>Mammary Neoplasms, Experimental - therapy</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Neovascularization, Pathologic - prevention & control</subject><subject>Proto-Oncogene Proteins c-met - genetics</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtPHDEUhS2UKBCSH0CDXEU0M_Fj_FilihCQSESREKktj30HvNqxF9uDtP8eo12JjlT3Ft85xfkQOqOkp4TK7-veudwzQoaeiJ5wdoROqFa641LLD-0XXHSSEn2MPpeyJi1D1eoTOqaCSUoHdoLu7m1-gBriA66PgOsyp4xt9DjUgufgcoL4HHKKM8SKxx222C92001LdDWkiD24tMN_oOIMDrY15S_o42Q3Bb4e7in6d311f_mru_178_vy523nBGO188Q5ovxIp4lbJwkbQDPhB6B2HIVSlLKJKKmI85oDCD4NEjwINo3cK834Kfq2793m9LRAqWYOxcFmYyOkpRgpFRv4sGrgxbtgm0zoga-0_m8nVVJTQlQD6R5sC5WSYTLbHGabd4YS8yrHrE2TY17lGCJMk9My54fyZZzBvyUONhrwYw9Am-05QDbFBYgOfGjjVuNTeKf-BSVln2g</recordid><startdate>20040701</startdate><enddate>20040701</enddate><creator>Michieli, Paolo</creator><creator>Mazzone, Massimiliano</creator><creator>Basilico, Cristina</creator><creator>Cavassa, Silvia</creator><creator>Sottile, Antonino</creator><creator>Naldini, Luigi</creator><creator>Comoglio, Paolo M</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20040701</creationdate><title>Targeting the tumor and its microenvironment by a dual-function decoy Met receptor</title><author>Michieli, Paolo ; 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We engineered a soluble Met receptor (decoy Met) that interferes with both HGF binding to Met and Met homodimerization. By lentiviral vector technology, we achieved local or systemic delivery of decoy Met in mice. We provide evidence that in vivo expression of decoy Met (1) inhibits tumor cell proliferation and survival in a variety of human xenografts, (2) impairs tumor angiogenesis by preventing host vessel arborization, (3) suppresses or prevents the formation of spontaneous metastases, and (4) synergizes with radiotherapy in inducing tumor regression, without (5) affecting housekeeping physiological functions in the adult animal.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15261142</pmid><doi>10.1016/j.ccr.2004.05.032</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Angiogenesis Inhibitors - pharmacology Animals Dimerization Disease-Free Survival Female Gene Transfer Techniques Genetic Therapy Genetic Vectors Hepatocyte Growth Factor - genetics Hepatocyte Growth Factor - metabolism Humans Lentivirus - genetics Lung Neoplasms - metabolism Lung Neoplasms - secondary Lung Neoplasms - therapy Mammary Neoplasms, Experimental - metabolism Mammary Neoplasms, Experimental - pathology Mammary Neoplasms, Experimental - therapy Mice Mice, Nude Neoplasm Invasiveness - pathology Neoplasm Invasiveness - prevention & control Neovascularization, Pathologic - prevention & control Proto-Oncogene Proteins c-met - genetics Proto-Oncogene Proteins c-met - metabolism Tumor Cells, Cultured Xenograft Model Antitumor Assays |
| title | Targeting the tumor and its microenvironment by a dual-function decoy Met receptor |
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