IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth
Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription factor MYC-N amplification. Previous stud...
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| Veröffentlicht in: | Anticancer research 2008-05, Vol.28 (3A), p.1509-1516 |
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| creator | COULTER, Don W BLATT, Julie D'ERCOLE, A. Joseph MOATS-STAATS, Billie M |
| description | Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis
of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription
factor MYC-N amplification. Previous studies have shown that MYC-N expression is disrupted by blockade of the IGF1R with a
specific monoclonal antibody, αIR3. Inhibition of IGF1R signaling can be accomplished by other agents, including rapamycin
or temsirolimus, which target mTOR (mammalian target of rapamycin). Materials and Methods: BE-2(c) and IMR-32 neuroblastoma
cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus alone or in combination and the viable
cells were counted. Results: Blockade of IGF1R signaling significantly inhibited cell growth as compared to untreated controls
(p |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_69314961</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20823394</sourcerecordid><originalsourceid>FETCH-LOGICAL-h301t-b87eb562f8c8aec8b5a398daccb91e0c6dfbfcf26ba244c0dd7c07b228dfe2b43</originalsourceid><addsrcrecordid>eNqF0M1LwzAYBvAiipvTf0Fy0VshH02aHkdxszAUxjyXfNVGmmYmLWP_vRU38ebpvfyeh4f3IpmjvEBpTgm8TOYQU5jmENJZchPjB4SMFZxcJzPEGYEU0nmiq_UqrcDWKLMffABV31ppB-t7UHonbW80ONihBVuxF-6obA8mtTMu2uA768Z4jkTwYsbgZSfi4J0Apek6sA7-MLS3yVUjumjuTneRvK2eduVzunldV-Vyk7YEoiGVPDeSMtxwxYVRXFJBCq6FUrJABiqmG9moBjMpcJYpqHWuYC4x5roxWGZkkTz-9O6D_xxNHGpno5p2iN74MdasICgrGPoXYsgxIcV34_0JjtIZXe-DdSIc6_MDJ_BwAiIq0TVB9MrGX4dhllHE_0xr7Xt7sMHU0Ymum2pJLQLmNVnWiMKCfAEqi4ke</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20823394</pqid></control><display><type>article</type><title>IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>COULTER, Don W ; BLATT, Julie ; D'ERCOLE, A. Joseph ; MOATS-STAATS, Billie M</creator><creatorcontrib>COULTER, Don W ; BLATT, Julie ; D'ERCOLE, A. Joseph ; MOATS-STAATS, Billie M</creatorcontrib><description>Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis
of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription
factor MYC-N amplification. Previous studies have shown that MYC-N expression is disrupted by blockade of the IGF1R with a
specific monoclonal antibody, αIR3. Inhibition of IGF1R signaling can be accomplished by other agents, including rapamycin
or temsirolimus, which target mTOR (mammalian target of rapamycin). Materials and Methods: BE-2(c) and IMR-32 neuroblastoma
cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus alone or in combination and the viable
cells were counted. Results: Blockade of IGF1R signaling significantly inhibited cell growth as compared to untreated controls
(p<0.05), and a combination of agents was more effective than each agent alone. Conclusion: The combination of rapamycin or
temsirolimus with αIR3 blocks the IGF1R signaling pathway and has an antiproliferative effect on neuroblastoma cells warranting
further investigations using inhibitors of IGF1R signaling as novel combination therapy for neuroblastoma.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 18630505</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Biological and medical sciences ; Cell Growth Processes - drug effects ; Cell Growth Processes - physiology ; Cell Line, Tumor ; Humans ; Medical sciences ; Neuroblastoma - drug therapy ; Neuroblastoma - metabolism ; Neuroblastoma - pathology ; Neurology ; Protein Kinases - metabolism ; Receptor, IGF Type 1 - antagonists & inhibitors ; Receptor, IGF Type 1 - metabolism ; Signal Transduction - drug effects ; Sirolimus - administration & dosage ; Sirolimus - analogs & derivatives ; Sirolimus - pharmacology ; TOR Serine-Threonine Kinases ; Tumors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Anticancer research, 2008-05, Vol.28 (3A), p.1509-1516</ispartof><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20445184$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18630505$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>COULTER, Don W</creatorcontrib><creatorcontrib>BLATT, Julie</creatorcontrib><creatorcontrib>D'ERCOLE, A. Joseph</creatorcontrib><creatorcontrib>MOATS-STAATS, Billie M</creatorcontrib><title>IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis
of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription
factor MYC-N amplification. Previous studies have shown that MYC-N expression is disrupted by blockade of the IGF1R with a
specific monoclonal antibody, αIR3. Inhibition of IGF1R signaling can be accomplished by other agents, including rapamycin
or temsirolimus, which target mTOR (mammalian target of rapamycin). Materials and Methods: BE-2(c) and IMR-32 neuroblastoma
cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus alone or in combination and the viable
cells were counted. Results: Blockade of IGF1R signaling significantly inhibited cell growth as compared to untreated controls
(p<0.05), and a combination of agents was more effective than each agent alone. Conclusion: The combination of rapamycin or
temsirolimus with αIR3 blocks the IGF1R signaling pathway and has an antiproliferative effect on neuroblastoma cells warranting
further investigations using inhibitors of IGF1R signaling as novel combination therapy for neuroblastoma.</description><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Growth Processes - drug effects</subject><subject>Cell Growth Processes - physiology</subject><subject>Cell Line, Tumor</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Neuroblastoma - drug therapy</subject><subject>Neuroblastoma - metabolism</subject><subject>Neuroblastoma - pathology</subject><subject>Neurology</subject><subject>Protein Kinases - metabolism</subject><subject>Receptor, IGF Type 1 - antagonists & inhibitors</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Sirolimus - administration & dosage</subject><subject>Sirolimus - analogs & derivatives</subject><subject>Sirolimus - pharmacology</subject><subject>TOR Serine-Threonine Kinases</subject><subject>Tumors</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0M1LwzAYBvAiipvTf0Fy0VshH02aHkdxszAUxjyXfNVGmmYmLWP_vRU38ebpvfyeh4f3IpmjvEBpTgm8TOYQU5jmENJZchPjB4SMFZxcJzPEGYEU0nmiq_UqrcDWKLMffABV31ppB-t7UHonbW80ONihBVuxF-6obA8mtTMu2uA768Z4jkTwYsbgZSfi4J0Apek6sA7-MLS3yVUjumjuTneRvK2eduVzunldV-Vyk7YEoiGVPDeSMtxwxYVRXFJBCq6FUrJABiqmG9moBjMpcJYpqHWuYC4x5roxWGZkkTz-9O6D_xxNHGpno5p2iN74MdasICgrGPoXYsgxIcV34_0JjtIZXe-DdSIc6_MDJ_BwAiIq0TVB9MrGX4dhllHE_0xr7Xt7sMHU0Ymum2pJLQLmNVnWiMKCfAEqi4ke</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>COULTER, Don W</creator><creator>BLATT, Julie</creator><creator>D'ERCOLE, A. Joseph</creator><creator>MOATS-STAATS, Billie M</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20080501</creationdate><title>IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth</title><author>COULTER, Don W ; BLATT, Julie ; D'ERCOLE, A. Joseph ; MOATS-STAATS, Billie M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h301t-b87eb562f8c8aec8b5a398daccb91e0c6dfbfcf26ba244c0dd7c07b228dfe2b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Growth Processes - drug effects</topic><topic>Cell Growth Processes - physiology</topic><topic>Cell Line, Tumor</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Neuroblastoma - drug therapy</topic><topic>Neuroblastoma - metabolism</topic><topic>Neuroblastoma - pathology</topic><topic>Neurology</topic><topic>Protein Kinases - metabolism</topic><topic>Receptor, IGF Type 1 - antagonists & inhibitors</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Sirolimus - administration & dosage</topic><topic>Sirolimus - analogs & derivatives</topic><topic>Sirolimus - pharmacology</topic><topic>TOR Serine-Threonine Kinases</topic><topic>Tumors</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>COULTER, Don W</creatorcontrib><creatorcontrib>BLATT, Julie</creatorcontrib><creatorcontrib>D'ERCOLE, A. Joseph</creatorcontrib><creatorcontrib>MOATS-STAATS, Billie 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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>COULTER, Don W</au><au>BLATT, Julie</au><au>D'ERCOLE, A. Joseph</au><au>MOATS-STAATS, Billie M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>28</volume><issue>3A</issue><spage>1509</spage><epage>1516</epage><pages>1509-1516</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis
of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription
factor MYC-N amplification. Previous studies have shown that MYC-N expression is disrupted by blockade of the IGF1R with a
specific monoclonal antibody, αIR3. Inhibition of IGF1R signaling can be accomplished by other agents, including rapamycin
or temsirolimus, which target mTOR (mammalian target of rapamycin). Materials and Methods: BE-2(c) and IMR-32 neuroblastoma
cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus alone or in combination and the viable
cells were counted. Results: Blockade of IGF1R signaling significantly inhibited cell growth as compared to untreated controls
(p<0.05), and a combination of agents was more effective than each agent alone. Conclusion: The combination of rapamycin or
temsirolimus with αIR3 blocks the IGF1R signaling pathway and has an antiproliferative effect on neuroblastoma cells warranting
further investigations using inhibitors of IGF1R signaling as novel combination therapy for neuroblastoma.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>18630505</pmid><tpages>8</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Antineoplastic Combined Chemotherapy Protocols - pharmacology Biological and medical sciences Cell Growth Processes - drug effects Cell Growth Processes - physiology Cell Line, Tumor Humans Medical sciences Neuroblastoma - drug therapy Neuroblastoma - metabolism Neuroblastoma - pathology Neurology Protein Kinases - metabolism Receptor, IGF Type 1 - antagonists & inhibitors Receptor, IGF Type 1 - metabolism Signal Transduction - drug effects Sirolimus - administration & dosage Sirolimus - analogs & derivatives Sirolimus - pharmacology TOR Serine-Threonine Kinases Tumors Tumors of the nervous system. Phacomatoses |
| title | IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth |
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