Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma
Purpose: Herstatin, an autoinhibitor of the epidermal growth factor (EGF) receptor family, was evaluated for efficacy against human glioblastoma in vitro and in vivo in a rat intracranial model. Experimental Design: Glioblastoma controlled by EGF receptor (EGFR; U87MG) or by the truncated mutant, ΔE...
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| Veröffentlicht in: | Clinical cancer research 2005-01, Vol.11 (1), p.335-340 |
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| creator | STAVEROSKY, Julia A MULDOON, Leslie L SHUHUA GUO EVANS, Adam J NEUWELT, Edward A CLINTON, Gail M |
| description | Purpose: Herstatin, an autoinhibitor of the epidermal growth factor (EGF) receptor family, was evaluated for efficacy against human
glioblastoma in vitro and in vivo in a rat intracranial model.
Experimental Design: Glioblastoma controlled by EGF receptor (EGFR; U87MG) or by the truncated mutant, ΔEGFR (U87MG/Δ), were transfected with
Herstatin and evaluated for in vitro and in vivo growth in nude rat brain. Cells treated with purified Herstatin in vitro were evaluated for growth and signal transduction.
Results: Herstatin expression prevented tumor formation by U87MG and purified Herstatin inhibited their growth in vitro in a dose-responsive fashion, whereas in vivo and in vitro growth of U87MG/Δ was resistant to Herstatin. Inhibition of U87MG growth correlated with suppressed EGF activation of EGFR
and of Akt but not mitogen-activated protein kinase signaling pathways, whereas ΔEGFR activity and intracellular signaling
in U87MG/Δ were unaffected by Herstatin treatment.
Conclusions: Herstatin may have utility against glioblastoma driven by the EGFR but not the mutant ΔEGFR. Blockade of Akt but not the
mitogen-activated protein kinase signaling cascade appears to be critical for suppression of intracranial tumor growth. |
| doi_str_mv | 10.1158/1078-0432.335.11.1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67379736</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67379736</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-c602639091ca6ce016084d11fac60c7ed3964f9aab18fa53e4bbbafb59314ac03</originalsourceid><addsrcrecordid>eNqFkU9vEzEQxS0EoqXwBTggX_gndYMnXtu7x1IlaaVKSAjO1qzjZQ3edbAdVb3x0fE2QTlysGzP_N4b6Q0hr4EtAETzCZhqKlbz5YJzUUoLeELOQQhV8aUUT8v7H3BGXqT0kzGogdXPyRkIqcqpz8mfGxtTxuymS4oTvdrn4KbBdS6HSENP82Dpaue2No7o6SaG-zzQNZq5_WG1WX-kX62xu_m7xtH5h0v62QfzKz0qb6cc0USc3ElcTDfehc5jymHEl-RZjz7ZV8f7gnxfr75d31R3Xza311d3lRGszpWRbCl5y1owKI1lIFlTbwF6LB2j7Ja3su5bxA6aHgW3ddd12Hei5VCjYfyCvDv47mL4vbcp69ElY73HyYZ90lJx1Sou_wuC4sBFM4PLA2hiSCnaXu-iGzE-aGB6XpCe89dz_rosqJQ0FNGbo_u-G-32JDlupABvjwAmg74v4RmXTlxBGqVE4d4fuMH9GO5dtNoU0sZok8Vohsdx81z-FwJzpnI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17313586</pqid></control><display><type>article</type><title>Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>American Association for Cancer Research</source><source>Alma/SFX Local Collection</source><creator>STAVEROSKY, Julia A ; MULDOON, Leslie L ; SHUHUA GUO ; EVANS, Adam J ; NEUWELT, Edward A ; CLINTON, Gail M</creator><creatorcontrib>STAVEROSKY, Julia A ; MULDOON, Leslie L ; SHUHUA GUO ; EVANS, Adam J ; NEUWELT, Edward A ; CLINTON, Gail M</creatorcontrib><description>Purpose: Herstatin, an autoinhibitor of the epidermal growth factor (EGF) receptor family, was evaluated for efficacy against human
glioblastoma in vitro and in vivo in a rat intracranial model.
Experimental Design: Glioblastoma controlled by EGF receptor (EGFR; U87MG) or by the truncated mutant, ΔEGFR (U87MG/Δ), were transfected with
Herstatin and evaluated for in vitro and in vivo growth in nude rat brain. Cells treated with purified Herstatin in vitro were evaluated for growth and signal transduction.
Results: Herstatin expression prevented tumor formation by U87MG and purified Herstatin inhibited their growth in vitro in a dose-responsive fashion, whereas in vivo and in vitro growth of U87MG/Δ was resistant to Herstatin. Inhibition of U87MG growth correlated with suppressed EGF activation of EGFR
and of Akt but not mitogen-activated protein kinase signaling pathways, whereas ΔEGFR activity and intracellular signaling
in U87MG/Δ were unaffected by Herstatin treatment.
Conclusions: Herstatin may have utility against glioblastoma driven by the EGFR but not the mutant ΔEGFR. Blockade of Akt but not the
mitogen-activated protein kinase signaling cascade appears to be critical for suppression of intracranial tumor growth.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.335.11.1</identifier><identifier>PMID: 15671564</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Western ; Brain - metabolism ; Brain Neoplasms - metabolism ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Dose-Response Relationship, Drug ; Epidermal Growth Factor Receptor ; Female ; Glioblastoma - drug therapy ; Glioblastoma - metabolism ; Herstatin ; Humans ; Immunohistochemistry ; In Vitro Techniques ; Insecta ; Intercellular Signaling Peptides and Proteins - metabolism ; Intercellular Signaling Peptides and Proteins - pharmacology ; Intracerebral Xenograft Model ; Medical sciences ; Neoplasm Transplantation ; Neurology ; Pharmacology. Drug treatments ; Phosphorylation ; Protein-Serine-Threonine Kinases - metabolism ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Nude ; Receptor, Epidermal Growth Factor - metabolism ; Receptor, ErbB-2 - metabolism ; Signal Transduction ; Time Factors ; Transfection ; Tumors of the nervous system. Phacomatoses ; ΔEGFR</subject><ispartof>Clinical cancer research, 2005-01, Vol.11 (1), p.335-340</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-c602639091ca6ce016084d11fac60c7ed3964f9aab18fa53e4bbbafb59314ac03</citedby><cites>FETCH-LOGICAL-c504t-c602639091ca6ce016084d11fac60c7ed3964f9aab18fa53e4bbbafb59314ac03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16438775$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15671564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STAVEROSKY, Julia A</creatorcontrib><creatorcontrib>MULDOON, Leslie L</creatorcontrib><creatorcontrib>SHUHUA GUO</creatorcontrib><creatorcontrib>EVANS, Adam J</creatorcontrib><creatorcontrib>NEUWELT, Edward A</creatorcontrib><creatorcontrib>CLINTON, Gail M</creatorcontrib><title>Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Herstatin, an autoinhibitor of the epidermal growth factor (EGF) receptor family, was evaluated for efficacy against human
glioblastoma in vitro and in vivo in a rat intracranial model.
Experimental Design: Glioblastoma controlled by EGF receptor (EGFR; U87MG) or by the truncated mutant, ΔEGFR (U87MG/Δ), were transfected with
Herstatin and evaluated for in vitro and in vivo growth in nude rat brain. Cells treated with purified Herstatin in vitro were evaluated for growth and signal transduction.
Results: Herstatin expression prevented tumor formation by U87MG and purified Herstatin inhibited their growth in vitro in a dose-responsive fashion, whereas in vivo and in vitro growth of U87MG/Δ was resistant to Herstatin. Inhibition of U87MG growth correlated with suppressed EGF activation of EGFR
and of Akt but not mitogen-activated protein kinase signaling pathways, whereas ΔEGFR activity and intracellular signaling
in U87MG/Δ were unaffected by Herstatin treatment.
Conclusions: Herstatin may have utility against glioblastoma driven by the EGFR but not the mutant ΔEGFR. Blockade of Akt but not the
mitogen-activated protein kinase signaling cascade appears to be critical for suppression of intracranial tumor growth.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Brain - metabolism</subject><subject>Brain Neoplasms - metabolism</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Epidermal Growth Factor Receptor</subject><subject>Female</subject><subject>Glioblastoma - drug therapy</subject><subject>Glioblastoma - metabolism</subject><subject>Herstatin</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Vitro Techniques</subject><subject>Insecta</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - pharmacology</subject><subject>Intracerebral Xenograft Model</subject><subject>Medical sciences</subject><subject>Neoplasm Transplantation</subject><subject>Neurology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Rats</subject><subject>Rats, Nude</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Signal Transduction</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Tumors of the nervous system. Phacomatoses</subject><subject>ΔEGFR</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9vEzEQxS0EoqXwBTggX_gndYMnXtu7x1IlaaVKSAjO1qzjZQ3edbAdVb3x0fE2QTlysGzP_N4b6Q0hr4EtAETzCZhqKlbz5YJzUUoLeELOQQhV8aUUT8v7H3BGXqT0kzGogdXPyRkIqcqpz8mfGxtTxuymS4oTvdrn4KbBdS6HSENP82Dpaue2No7o6SaG-zzQNZq5_WG1WX-kX62xu_m7xtH5h0v62QfzKz0qb6cc0USc3ElcTDfehc5jymHEl-RZjz7ZV8f7gnxfr75d31R3Xza311d3lRGszpWRbCl5y1owKI1lIFlTbwF6LB2j7Ja3su5bxA6aHgW3ddd12Hei5VCjYfyCvDv47mL4vbcp69ElY73HyYZ90lJx1Sou_wuC4sBFM4PLA2hiSCnaXu-iGzE-aGB6XpCe89dz_rosqJQ0FNGbo_u-G-32JDlupABvjwAmg74v4RmXTlxBGqVE4d4fuMH9GO5dtNoU0sZok8Vohsdx81z-FwJzpnI</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>STAVEROSKY, Julia A</creator><creator>MULDOON, Leslie L</creator><creator>SHUHUA GUO</creator><creator>EVANS, Adam J</creator><creator>NEUWELT, Edward A</creator><creator>CLINTON, Gail M</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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050101</creationdate><title>Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma</title><author>STAVEROSKY, Julia A ; MULDOON, Leslie L ; SHUHUA GUO ; EVANS, Adam J ; NEUWELT, Edward A ; CLINTON, Gail M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-c602639091ca6ce016084d11fac60c7ed3964f9aab18fa53e4bbbafb59314ac03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Brain - metabolism</topic><topic>Brain Neoplasms - metabolism</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Dose-Response Relationship, Drug</topic><topic>Epidermal Growth Factor Receptor</topic><topic>Female</topic><topic>Glioblastoma - drug therapy</topic><topic>Glioblastoma - metabolism</topic><topic>Herstatin</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Vitro Techniques</topic><topic>Insecta</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Intercellular Signaling Peptides and Proteins - pharmacology</topic><topic>Intracerebral Xenograft Model</topic><topic>Medical sciences</topic><topic>Neoplasm Transplantation</topic><topic>Neurology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Rats</topic><topic>Rats, Nude</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Signal Transduction</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Tumors of the nervous system. Phacomatoses</topic><topic>ΔEGFR</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STAVEROSKY, Julia A</creatorcontrib><creatorcontrib>MULDOON, Leslie L</creatorcontrib><creatorcontrib>SHUHUA GUO</creatorcontrib><creatorcontrib>EVANS, Adam J</creatorcontrib><creatorcontrib>NEUWELT, Edward A</creatorcontrib><creatorcontrib>CLINTON, Gail M</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STAVEROSKY, Julia A</au><au>MULDOON, Leslie L</au><au>SHUHUA GUO</au><au>EVANS, Adam J</au><au>NEUWELT, Edward A</au><au>CLINTON, Gail M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>11</volume><issue>1</issue><spage>335</spage><epage>340</epage><pages>335-340</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Herstatin, an autoinhibitor of the epidermal growth factor (EGF) receptor family, was evaluated for efficacy against human
glioblastoma in vitro and in vivo in a rat intracranial model.
Experimental Design: Glioblastoma controlled by EGF receptor (EGFR; U87MG) or by the truncated mutant, ΔEGFR (U87MG/Δ), were transfected with
Herstatin and evaluated for in vitro and in vivo growth in nude rat brain. Cells treated with purified Herstatin in vitro were evaluated for growth and signal transduction.
Results: Herstatin expression prevented tumor formation by U87MG and purified Herstatin inhibited their growth in vitro in a dose-responsive fashion, whereas in vivo and in vitro growth of U87MG/Δ was resistant to Herstatin. Inhibition of U87MG growth correlated with suppressed EGF activation of EGFR
and of Akt but not mitogen-activated protein kinase signaling pathways, whereas ΔEGFR activity and intracellular signaling
in U87MG/Δ were unaffected by Herstatin treatment.
Conclusions: Herstatin may have utility against glioblastoma driven by the EGFR but not the mutant ΔEGFR. Blockade of Akt but not the
mitogen-activated protein kinase signaling cascade appears to be critical for suppression of intracranial tumor growth.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15671564</pmid><doi>10.1158/1078-0432.335.11.1</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2005-01, Vol.11 (1), p.335-340 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic agents Biological and medical sciences Blotting, Western Brain - metabolism Brain Neoplasms - metabolism Cell Line Cell Line, Tumor Cell Proliferation Dose-Response Relationship, Drug Epidermal Growth Factor Receptor Female Glioblastoma - drug therapy Glioblastoma - metabolism Herstatin Humans Immunohistochemistry In Vitro Techniques Insecta Intercellular Signaling Peptides and Proteins - metabolism Intercellular Signaling Peptides and Proteins - pharmacology Intracerebral Xenograft Model Medical sciences Neoplasm Transplantation Neurology Pharmacology. Drug treatments Phosphorylation Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-akt Rats Rats, Nude Receptor, Epidermal Growth Factor - metabolism Receptor, ErbB-2 - metabolism Signal Transduction Time Factors Transfection Tumors of the nervous system. Phacomatoses ΔEGFR |
| title | Herstatin, an Autoinhibitor of the Epidermal Growth Factor (EGF) Receptor Family, Blocks the Intracranial Growth of Glioblastoma |
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