Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer
Purpose: The eukaryotic translation initiation factor complex 4E (eIF4E) is downstream in the mammalian target of rapamycin (mTOR) pathway. This study explored expression of eIF4E and its relationship with the PTEN/AKT and RAS/MEK/ERK pathways in non–small cell lung carcinoma (NSCLC). Experimental D...
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| Veröffentlicht in: | Clinical cancer research 2010-01, Vol.16 (1), p.240-248 |
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| creator | Yoshizawa, Akihiko Fukuoka, Junya Shimizu, Shigeki Shilo, Konstantin Franks, Teri J Hewitt, Stephen M Fujii, Takeshi Cordon-Cardo, Carlos Jen, Jin Travis, William D |
| description | Purpose: The eukaryotic translation initiation factor complex 4E (eIF4E) is downstream in the mammalian target of rapamycin (mTOR)
pathway. This study explored expression of eIF4E and its relationship with the PTEN/AKT and RAS/MEK/ERK pathways in non–small
cell lung carcinoma (NSCLC).
Experimental Design: The status of phosphorylated eIF4E (p-eIF4E), phosphorylated AKT (p-AKT), PTEN, phosphorylated tuberin (p-TSC2), phosphorylated
mTOR (p-mTOR), phosphorylated S6 (p-S6), and phosphorylated Erk1/2 (p-Erk1/2) was studied using immunohistochemical analysis
applied to a tissue microarray containing 300 NSCLCs. Staining results for each antibody were compared with clinical and pathologic
features, and the relationship between staining results was explored.
Results: Overexpression of p-eIF4E, p-AKT, p-TSC2, p-mTOR, p-S6, and p-Erk1/2 in NSCLC was found in 39.9%, 78.8%, 5.1%, 46.7%, 27.1%,
and 16.6% of tumors, respectively. The phenotype of p-eIF4E correlated positively with that of p-AKT, p-TSC2, and p-S6 ( P < 0.001). Overall survival in NSCLC patients was significantly shorter in cases with overexpression of p-eIF4E and p-AKT
alone and in combination (log-rank P < 0.001, each). Cases with underexpression of PTEN were limited (6.4%), and this phenotype did not correlate with any clinical
variable. In cluster analysis, the p-AKT/p-mTOR/p-eIF4E/p-S6–positive group had significantly shorter survival compared with
the survival of all cases ( P < 0.001). Multivariate analysis showed that p-eIF4E overexpression is an independent prognostic factor for NSCLC ( P = 0.004).
Conclusions: This study shows that p-eIF4E expression in addition to p-AKT predicts poor prognosis in NSCLC. Moreover, the correlation
between expression of p-eIF4E with p-AKT, as well as p-TSC2 and p-S6, indicates that eIF4E activation through the AKT pathway
plays an important role in the progression of NSCLC. Clin Cancer Res; 16(1); OF1–9 |
| doi_str_mv | 10.1158/1078-0432.CCR-09-0986 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7581274</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>733888719</sourcerecordid><originalsourceid>FETCH-LOGICAL-c524t-f87cdf3c150a7ba796a723e4221dbbfac3829cc1a1f3547d6b64e1c3b5138a7c3</originalsourceid><addsrcrecordid>eNpVkd1u0zAUgCMEYmPwCCDfoF1l-Dd2bpCqaIOKik1sXFsnrlMbpXGxk5bd8Q68IU-Cy7oNJMu25O_8-HxF8ZrgM0KEekewVCXmjJ41zZcS13mp6klxTISQJaOVeJrv98xR8SKlbxgTTjB_XhxRjLFSrD4uwuXWRvtjE21KPgwodOjKhbRxobTzC36O5gnNUgrGw2iXaOdHh66nuPVb6NHoYphWDs0-3aArGN0ObpEf0Ocw_P7563oNfY8am7fFNKxQA4Ox8WXxrIM-2VeH86T4enF-03wsF5cf5s1sURpB-Vh2SpplxwwRGGQLsq5AUmY5pWTZth0YpmhtDAHSMcHlsmorbolhrSBMgTTspHh_l3cztWu7NHYYI_R6E_0a4q0O4PX_L4N3ehW2WgpFqOQ5wekhQQzfJ5tGvfbJ5N_AYMOUtGRMKSVJnUlxR5oYUoq2e6hCsN670nsPeu9BZ1ca13rvKse9-bfFh6h7ORl4ewAgGei7mCfo0yNHOcaCscdWnV-5nY9Wm7-zzk4tROM0qTTRmWZ_AKQxrRU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>733888719</pqid></control><display><type>article</type><title>Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Yoshizawa, Akihiko ; Fukuoka, Junya ; Shimizu, Shigeki ; Shilo, Konstantin ; Franks, Teri J ; Hewitt, Stephen M ; Fujii, Takeshi ; Cordon-Cardo, Carlos ; Jen, Jin ; Travis, William D</creator><creatorcontrib>Yoshizawa, Akihiko ; Fukuoka, Junya ; Shimizu, Shigeki ; Shilo, Konstantin ; Franks, Teri J ; Hewitt, Stephen M ; Fujii, Takeshi ; Cordon-Cardo, Carlos ; Jen, Jin ; Travis, William D</creatorcontrib><description>Purpose: The eukaryotic translation initiation factor complex 4E (eIF4E) is downstream in the mammalian target of rapamycin (mTOR)
pathway. This study explored expression of eIF4E and its relationship with the PTEN/AKT and RAS/MEK/ERK pathways in non–small
cell lung carcinoma (NSCLC).
Experimental Design: The status of phosphorylated eIF4E (p-eIF4E), phosphorylated AKT (p-AKT), PTEN, phosphorylated tuberin (p-TSC2), phosphorylated
mTOR (p-mTOR), phosphorylated S6 (p-S6), and phosphorylated Erk1/2 (p-Erk1/2) was studied using immunohistochemical analysis
applied to a tissue microarray containing 300 NSCLCs. Staining results for each antibody were compared with clinical and pathologic
features, and the relationship between staining results was explored.
Results: Overexpression of p-eIF4E, p-AKT, p-TSC2, p-mTOR, p-S6, and p-Erk1/2 in NSCLC was found in 39.9%, 78.8%, 5.1%, 46.7%, 27.1%,
and 16.6% of tumors, respectively. The phenotype of p-eIF4E correlated positively with that of p-AKT, p-TSC2, and p-S6 ( P < 0.001). Overall survival in NSCLC patients was significantly shorter in cases with overexpression of p-eIF4E and p-AKT
alone and in combination (log-rank P < 0.001, each). Cases with underexpression of PTEN were limited (6.4%), and this phenotype did not correlate with any clinical
variable. In cluster analysis, the p-AKT/p-mTOR/p-eIF4E/p-S6–positive group had significantly shorter survival compared with
the survival of all cases ( P < 0.001). Multivariate analysis showed that p-eIF4E overexpression is an independent prognostic factor for NSCLC ( P = 0.004).
Conclusions: This study shows that p-eIF4E expression in addition to p-AKT predicts poor prognosis in NSCLC. Moreover, the correlation
between expression of p-eIF4E with p-AKT, as well as p-TSC2 and p-S6, indicates that eIF4E activation through the AKT pathway
plays an important role in the progression of NSCLC. Clin Cancer Res; 16(1); OF1–9</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-09-0986</identifier><identifier>PMID: 20008839</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>AKT pathway ; Antineoplastic agents ; Biological and medical sciences ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - mortality ; eIF4E ; Erk1/2 ; Eukaryotic Initiation Factor-4E - metabolism ; Female ; Humans ; Lung Neoplasms - metabolism ; Lung Neoplasms - mortality ; Male ; Medical sciences ; Mitogen-Activated Protein Kinase 3 - metabolism ; non–small cell lung cancer ; Pharmacology. Drug treatments ; Phosphorylation ; Pneumology ; Prognosis ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - metabolism ; Signal Transduction ; Tissue Array Analysis ; Tumors of the respiratory system and mediastinum</subject><ispartof>Clinical cancer research, 2010-01, Vol.16 (1), p.240-248</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-f87cdf3c150a7ba796a723e4221dbbfac3829cc1a1f3547d6b64e1c3b5138a7c3</citedby><cites>FETCH-LOGICAL-c524t-f87cdf3c150a7ba796a723e4221dbbfac3829cc1a1f3547d6b64e1c3b5138a7c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22400533$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20008839$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshizawa, Akihiko</creatorcontrib><creatorcontrib>Fukuoka, Junya</creatorcontrib><creatorcontrib>Shimizu, Shigeki</creatorcontrib><creatorcontrib>Shilo, Konstantin</creatorcontrib><creatorcontrib>Franks, Teri J</creatorcontrib><creatorcontrib>Hewitt, Stephen M</creatorcontrib><creatorcontrib>Fujii, Takeshi</creatorcontrib><creatorcontrib>Cordon-Cardo, Carlos</creatorcontrib><creatorcontrib>Jen, Jin</creatorcontrib><creatorcontrib>Travis, William D</creatorcontrib><title>Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: The eukaryotic translation initiation factor complex 4E (eIF4E) is downstream in the mammalian target of rapamycin (mTOR)
pathway. This study explored expression of eIF4E and its relationship with the PTEN/AKT and RAS/MEK/ERK pathways in non–small
cell lung carcinoma (NSCLC).
Experimental Design: The status of phosphorylated eIF4E (p-eIF4E), phosphorylated AKT (p-AKT), PTEN, phosphorylated tuberin (p-TSC2), phosphorylated
mTOR (p-mTOR), phosphorylated S6 (p-S6), and phosphorylated Erk1/2 (p-Erk1/2) was studied using immunohistochemical analysis
applied to a tissue microarray containing 300 NSCLCs. Staining results for each antibody were compared with clinical and pathologic
features, and the relationship between staining results was explored.
Results: Overexpression of p-eIF4E, p-AKT, p-TSC2, p-mTOR, p-S6, and p-Erk1/2 in NSCLC was found in 39.9%, 78.8%, 5.1%, 46.7%, 27.1%,
and 16.6% of tumors, respectively. The phenotype of p-eIF4E correlated positively with that of p-AKT, p-TSC2, and p-S6 ( P < 0.001). Overall survival in NSCLC patients was significantly shorter in cases with overexpression of p-eIF4E and p-AKT
alone and in combination (log-rank P < 0.001, each). Cases with underexpression of PTEN were limited (6.4%), and this phenotype did not correlate with any clinical
variable. In cluster analysis, the p-AKT/p-mTOR/p-eIF4E/p-S6–positive group had significantly shorter survival compared with
the survival of all cases ( P < 0.001). Multivariate analysis showed that p-eIF4E overexpression is an independent prognostic factor for NSCLC ( P = 0.004).
Conclusions: This study shows that p-eIF4E expression in addition to p-AKT predicts poor prognosis in NSCLC. Moreover, the correlation
between expression of p-eIF4E with p-AKT, as well as p-TSC2 and p-S6, indicates that eIF4E activation through the AKT pathway
plays an important role in the progression of NSCLC. Clin Cancer Res; 16(1); OF1–9</description><subject>AKT pathway</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - mortality</subject><subject>eIF4E</subject><subject>Erk1/2</subject><subject>Eukaryotic Initiation Factor-4E - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - mortality</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>non–small cell lung cancer</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Pneumology</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Signal Transduction</subject><subject>Tissue Array Analysis</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkd1u0zAUgCMEYmPwCCDfoF1l-Dd2bpCqaIOKik1sXFsnrlMbpXGxk5bd8Q68IU-Cy7oNJMu25O_8-HxF8ZrgM0KEekewVCXmjJ41zZcS13mp6klxTISQJaOVeJrv98xR8SKlbxgTTjB_XhxRjLFSrD4uwuXWRvtjE21KPgwodOjKhbRxobTzC36O5gnNUgrGw2iXaOdHh66nuPVb6NHoYphWDs0-3aArGN0ObpEf0Ocw_P7563oNfY8am7fFNKxQA4Ox8WXxrIM-2VeH86T4enF-03wsF5cf5s1sURpB-Vh2SpplxwwRGGQLsq5AUmY5pWTZth0YpmhtDAHSMcHlsmorbolhrSBMgTTspHh_l3cztWu7NHYYI_R6E_0a4q0O4PX_L4N3ehW2WgpFqOQ5wekhQQzfJ5tGvfbJ5N_AYMOUtGRMKSVJnUlxR5oYUoq2e6hCsN670nsPeu9BZ1ca13rvKse9-bfFh6h7ORl4ewAgGei7mCfo0yNHOcaCscdWnV-5nY9Wm7-zzk4tROM0qTTRmWZ_AKQxrRU</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>Yoshizawa, Akihiko</creator><creator>Fukuoka, Junya</creator><creator>Shimizu, Shigeki</creator><creator>Shilo, Konstantin</creator><creator>Franks, Teri J</creator><creator>Hewitt, Stephen M</creator><creator>Fujii, Takeshi</creator><creator>Cordon-Cardo, Carlos</creator><creator>Jen, Jin</creator><creator>Travis, William D</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100101</creationdate><title>Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer</title><author>Yoshizawa, Akihiko ; Fukuoka, Junya ; Shimizu, Shigeki ; Shilo, Konstantin ; Franks, Teri J ; Hewitt, Stephen M ; Fujii, Takeshi ; Cordon-Cardo, Carlos ; Jen, Jin ; Travis, William D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-f87cdf3c150a7ba796a723e4221dbbfac3829cc1a1f3547d6b64e1c3b5138a7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>AKT pathway</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - mortality</topic><topic>eIF4E</topic><topic>Erk1/2</topic><topic>Eukaryotic Initiation Factor-4E - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - mortality</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>non–small cell lung cancer</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphorylation</topic><topic>Pneumology</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Signal Transduction</topic><topic>Tissue Array Analysis</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshizawa, Akihiko</creatorcontrib><creatorcontrib>Fukuoka, Junya</creatorcontrib><creatorcontrib>Shimizu, Shigeki</creatorcontrib><creatorcontrib>Shilo, Konstantin</creatorcontrib><creatorcontrib>Franks, Teri J</creatorcontrib><creatorcontrib>Hewitt, Stephen M</creatorcontrib><creatorcontrib>Fujii, Takeshi</creatorcontrib><creatorcontrib>Cordon-Cardo, Carlos</creatorcontrib><creatorcontrib>Jen, Jin</creatorcontrib><creatorcontrib>Travis, William D</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshizawa, Akihiko</au><au>Fukuoka, Junya</au><au>Shimizu, Shigeki</au><au>Shilo, Konstantin</au><au>Franks, Teri J</au><au>Hewitt, Stephen M</au><au>Fujii, Takeshi</au><au>Cordon-Cardo, Carlos</au><au>Jen, Jin</au><au>Travis, William D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>16</volume><issue>1</issue><spage>240</spage><epage>248</epage><pages>240-248</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>Purpose: The eukaryotic translation initiation factor complex 4E (eIF4E) is downstream in the mammalian target of rapamycin (mTOR)
pathway. This study explored expression of eIF4E and its relationship with the PTEN/AKT and RAS/MEK/ERK pathways in non–small
cell lung carcinoma (NSCLC).
Experimental Design: The status of phosphorylated eIF4E (p-eIF4E), phosphorylated AKT (p-AKT), PTEN, phosphorylated tuberin (p-TSC2), phosphorylated
mTOR (p-mTOR), phosphorylated S6 (p-S6), and phosphorylated Erk1/2 (p-Erk1/2) was studied using immunohistochemical analysis
applied to a tissue microarray containing 300 NSCLCs. Staining results for each antibody were compared with clinical and pathologic
features, and the relationship between staining results was explored.
Results: Overexpression of p-eIF4E, p-AKT, p-TSC2, p-mTOR, p-S6, and p-Erk1/2 in NSCLC was found in 39.9%, 78.8%, 5.1%, 46.7%, 27.1%,
and 16.6% of tumors, respectively. The phenotype of p-eIF4E correlated positively with that of p-AKT, p-TSC2, and p-S6 ( P < 0.001). Overall survival in NSCLC patients was significantly shorter in cases with overexpression of p-eIF4E and p-AKT
alone and in combination (log-rank P < 0.001, each). Cases with underexpression of PTEN were limited (6.4%), and this phenotype did not correlate with any clinical
variable. In cluster analysis, the p-AKT/p-mTOR/p-eIF4E/p-S6–positive group had significantly shorter survival compared with
the survival of all cases ( P < 0.001). Multivariate analysis showed that p-eIF4E overexpression is an independent prognostic factor for NSCLC ( P = 0.004).
Conclusions: This study shows that p-eIF4E expression in addition to p-AKT predicts poor prognosis in NSCLC. Moreover, the correlation
between expression of p-eIF4E with p-AKT, as well as p-TSC2 and p-S6, indicates that eIF4E activation through the AKT pathway
plays an important role in the progression of NSCLC. Clin Cancer Res; 16(1); OF1–9</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>20008839</pmid><doi>10.1158/1078-0432.CCR-09-0986</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AKT pathway Antineoplastic agents Biological and medical sciences Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - mortality eIF4E Erk1/2 Eukaryotic Initiation Factor-4E - metabolism Female Humans Lung Neoplasms - metabolism Lung Neoplasms - mortality Male Medical sciences Mitogen-Activated Protein Kinase 3 - metabolism non–small cell lung cancer Pharmacology. Drug treatments Phosphorylation Pneumology Prognosis Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - metabolism Signal Transduction Tissue Array Analysis Tumors of the respiratory system and mediastinum |
| title | Overexpression of Phospho-eIF4E Is Associated with Survival through AKT Pathway in Non–Small Cell Lung Cancer |
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