The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer
The aim of this study was to investigate the consequences of insulin-like growth factors (IGF) and IGF receptor dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2005-01, Vol.32 (1), p.65-71 |
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| creator | Pavelic, Jasminka Krizanac, Simun Kapitanovic, Sanja Pavelic, Ljubomir Samarzija, Miroslav Pavicic, Fadila Spaventi, Sime Jakopovic, Marko Herceg-Ivanovi, Zlata Pavelic, Kresimir |
| description | The aim of this study was to investigate the consequences of insulin-like growth factors (IGF) and IGF receptor dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and adenocarcinomas. In 40% of informative adenocarcinomas expressing the highest values of IGF-2 and Ki-67 proteins, M6P/IGF-2R gene had LOH at one allele and a mutation in another allele. All four squamous cell carcinoma samples expressed LOH/mutation in the M6P/IGF-2R gene. The alphaIR3 strongly diminished proliferation and increased apoptosis in cultures established from squamous cell carcinomas overexpressing IGF-2 and IGF-1R. Telomerase activity was assessed in four squamous cell carcinomas. Cell treatment with IGF-1 increased telomerase activity. The opposite was observed when the cells were treated with alphaIR3, which inhibits the activity of IGF-1 receptors. Our findings suggest that disruption of the IGF/IGF receptors axis is involved in lung cancer formation. |
| doi_str_mv | 10.1165/rcmb.2004-0232OC |
| format | Article |
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A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and adenocarcinomas. In 40% of informative adenocarcinomas expressing the highest values of IGF-2 and Ki-67 proteins, M6P/IGF-2R gene had LOH at one allele and a mutation in another allele. All four squamous cell carcinoma samples expressed LOH/mutation in the M6P/IGF-2R gene. The alphaIR3 strongly diminished proliferation and increased apoptosis in cultures established from squamous cell carcinomas overexpressing IGF-2 and IGF-1R. Telomerase activity was assessed in four squamous cell carcinomas. Cell treatment with IGF-1 increased telomerase activity. The opposite was observed when the cells were treated with alphaIR3, which inhibits the activity of IGF-1 receptors. Our findings suggest that disruption of the IGF/IGF receptors axis is involved in lung cancer formation.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2004-0232OC</identifier><identifier>PMID: 15514114</identifier><identifier>CODEN: AJRBEL</identifier><language>eng</language><publisher>United States: Am Thoracic Soc</publisher><subject>Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Adult ; Aged ; Apoptosis - physiology ; Carcinoma, Large Cell - genetics ; Carcinoma, Large Cell - metabolism ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Female ; Humans ; Immunohistochemistry ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Male ; Middle Aged ; Receptors, Somatomedin - metabolism ; Somatomedins - metabolism ; Telomerase - metabolism ; Tumor Cells, Cultured</subject><ispartof>American journal of respiratory cell and molecular biology, 2005-01, Vol.32 (1), p.65-71</ispartof><rights>Copyright American Thoracic Society Jan 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-ec23e28d48cde4dbfc2b99ac589078a526f9eddefea8d6f215b85328ef6dc7e63</citedby><cites>FETCH-LOGICAL-c356t-ec23e28d48cde4dbfc2b99ac589078a526f9eddefea8d6f215b85328ef6dc7e63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15514114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pavelic, Jasminka</creatorcontrib><creatorcontrib>Krizanac, Simun</creatorcontrib><creatorcontrib>Kapitanovic, Sanja</creatorcontrib><creatorcontrib>Pavelic, Ljubomir</creatorcontrib><creatorcontrib>Samarzija, Miroslav</creatorcontrib><creatorcontrib>Pavicic, Fadila</creatorcontrib><creatorcontrib>Spaventi, Sime</creatorcontrib><creatorcontrib>Jakopovic, Marko</creatorcontrib><creatorcontrib>Herceg-Ivanovi, Zlata</creatorcontrib><creatorcontrib>Pavelic, Kresimir</creatorcontrib><title>The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>The aim of this study was to investigate the consequences of insulin-like growth factors (IGF) and IGF receptor dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and adenocarcinomas. In 40% of informative adenocarcinomas expressing the highest values of IGF-2 and Ki-67 proteins, M6P/IGF-2R gene had LOH at one allele and a mutation in another allele. All four squamous cell carcinoma samples expressed LOH/mutation in the M6P/IGF-2R gene. The alphaIR3 strongly diminished proliferation and increased apoptosis in cultures established from squamous cell carcinomas overexpressing IGF-2 and IGF-1R. Telomerase activity was assessed in four squamous cell carcinomas. Cell treatment with IGF-1 increased telomerase activity. The opposite was observed when the cells were treated with alphaIR3, which inhibits the activity of IGF-1 receptors. Our findings suggest that disruption of the IGF/IGF receptors axis is involved in lung cancer formation.</description><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis - physiology</subject><subject>Carcinoma, Large Cell - genetics</subject><subject>Carcinoma, Large Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Receptors, Somatomedin - metabolism</subject><subject>Somatomedins - metabolism</subject><subject>Telomerase - metabolism</subject><subject>Tumor Cells, Cultured</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkM9L5DAUgMOirL_2vicJHtZTNb8nPUrdUWFAWMZzSNMXp2ObjEmL-N9vywwInt47fO_j8SH0m5IbSpW8Ta6vbxghoiCMs-fqBzqlkstClLo8mnYiREGlKE_QWc5bQijTlP5EJ1RKKigVp2i93gCuYsjwPkJwkHH0-CnksWtDsWrfAD-k-DFs8NK6IaZ8-w8c7OYN339mPwY3tDHgNuDVGF5xZSdHukDH3nYZfh3mOXpZ_l1Xj8Xq-eGpulsVjks1FOAYB6YboV0Doqm9Y3VZWid1SRbaSqZ8CU0DHqxulGdU1lpypsGrxi1A8XP0Z-_dpTi9nwfTt9lB19kAccxGLThjWrEJvPoGbuOYwvSbYWShuBJstpE95FLMOYE3u9T2Nn0aSsyc28y5zZzb7HNPJ5cH71j30HwdHPpOwPUe2LSvm482gcm97boJp8ZuZx9nhhol-X9R8op-</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>Pavelic, Jasminka</creator><creator>Krizanac, Simun</creator><creator>Kapitanovic, Sanja</creator><creator>Pavelic, Ljubomir</creator><creator>Samarzija, Miroslav</creator><creator>Pavicic, Fadila</creator><creator>Spaventi, Sime</creator><creator>Jakopovic, Marko</creator><creator>Herceg-Ivanovi, Zlata</creator><creator>Pavelic, Kresimir</creator><general>Am Thoracic Soc</general><general>American Thoracic Society</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20050101</creationdate><title>The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer</title><author>Pavelic, Jasminka ; Krizanac, Simun ; Kapitanovic, Sanja ; Pavelic, Ljubomir ; Samarzija, Miroslav ; Pavicic, Fadila ; Spaventi, Sime ; Jakopovic, Marko ; Herceg-Ivanovi, Zlata ; Pavelic, Kresimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-ec23e28d48cde4dbfc2b99ac589078a526f9eddefea8d6f215b85328ef6dc7e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adenocarcinoma - 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Academic</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pavelic, Jasminka</au><au>Krizanac, Simun</au><au>Kapitanovic, Sanja</au><au>Pavelic, Ljubomir</au><au>Samarzija, Miroslav</au><au>Pavicic, Fadila</au><au>Spaventi, Sime</au><au>Jakopovic, Marko</au><au>Herceg-Ivanovi, Zlata</au><au>Pavelic, Kresimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>32</volume><issue>1</issue><spage>65</spage><epage>71</epage><pages>65-71</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><coden>AJRBEL</coden><abstract>The aim of this study was to investigate the consequences of insulin-like growth factors (IGF) and IGF receptor dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and adenocarcinomas. In 40% of informative adenocarcinomas expressing the highest values of IGF-2 and Ki-67 proteins, M6P/IGF-2R gene had LOH at one allele and a mutation in another allele. All four squamous cell carcinoma samples expressed LOH/mutation in the M6P/IGF-2R gene. The alphaIR3 strongly diminished proliferation and increased apoptosis in cultures established from squamous cell carcinomas overexpressing IGF-2 and IGF-1R. Telomerase activity was assessed in four squamous cell carcinomas. Cell treatment with IGF-1 increased telomerase activity. The opposite was observed when the cells were treated with alphaIR3, which inhibits the activity of IGF-1 receptors. Our findings suggest that disruption of the IGF/IGF receptors axis is involved in lung cancer formation.</abstract><cop>United States</cop><pub>Am Thoracic Soc</pub><pmid>15514114</pmid><doi>10.1165/rcmb.2004-0232OC</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 1044-1549 |
| ispartof | American journal of respiratory cell and molecular biology, 2005-01, Vol.32 (1), p.65-71 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library; Journals@Ovid Complete |
| subjects | Adenocarcinoma - genetics Adenocarcinoma - metabolism Adult Aged Apoptosis - physiology Carcinoma, Large Cell - genetics Carcinoma, Large Cell - metabolism Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Female Humans Immunohistochemistry Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Male Middle Aged Receptors, Somatomedin - metabolism Somatomedins - metabolism Telomerase - metabolism Tumor Cells, Cultured |
| title | The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer |
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