p-AKT overexpression in primary renal cell carcinomas and their metastases
In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluat...
Gespeichert in:
Veröffentlicht in: | Clinical & experimental metastasis 2010-12, Vol.27 (8), p.611-617 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 617 |
---|---|
container_issue | 8 |
container_start_page | 611 |
container_title | Clinical & experimental metastasis |
container_volume | 27 |
creator | Hager, Martina Haufe, Heike Lusuardi, Lukas Schmeller, Nikolaus Kolbitsch, Christian |
description | In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluated p-AKT expression in a tissue microarray of primary renal cell carcinomas (PRCCs) (n = 45), their metastases (primary onset n = 45, secondary onset n = 5), and normal renal parenchyma (n = 45) by means of immunohistochemistry. Total p-AKT overexpression was found in 24/45 (53.3%) PRCCs, in 32/45 (71.1%) primary and in 3/5 (60%) secondary onset metastases. Membranous p-AKT overexpression was seen more frequently in PRCCs, namely 11/45 (24.4%), than in primary onset metastases 1/45 (2.2%). Overexpression of total p-AKT solely in metastases without overexpression in PRCC was exclusively demonstrated in primary onset metastases, namely in 28.9%. Patients with total p-AKT overexpression in primary carcinomas showed a trend to longer, and those with total p-AKT overexpression in metastases a tendency to shorter survival. In conclusion, the present study shows total p-AKT overexpression to be more frequent in metastases than in PRCCs. Total p-AKT overexpression in metastases without concomitant overexpression in their primary tumors was found in approximately one-third of primary onset metastases, which is interesting with regard to the association between high p-AKT expression and sensitivity to mTOR inhibitor therapy. |
doi_str_mv | 10.1007/s10585-010-9351-y |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_762480487</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2202699771</sourcerecordid><originalsourceid>FETCH-LOGICAL-c394t-32c5f61d1f77df04ff70c43dd76ce0f5f626d4c69ea5eed31f18a8196cb690f73</originalsourceid><addsrcrecordid>eNp9kMtuFDEQRS0EIpPAB2QDrWyyMlTZbj-WUZQHEIkFydpy3OWko-nuwZ6JmL_Hox6CxAKp5FrUubdcl7FjhE8IYD4XhNa2HBC4ky3y7Su2wNZIboTRr9kChBYcrLMH7LCUJwBQxti37ECAVcpJXLCvK3727baZninTr1WmUvppbPqxWeV-CHnbZBrDsom0rE_IsR-nIZQmjF2zfqQ-NwOtQ6lF5R17k8Ky0Pt9P2J3lxe359f85vvVl_OzGx6lU2suRWyTxg6TMV0ClZKBqGTXGR0JUp0J3amoHYWWqJOY0AaLTsd77SAZecROZ99Vnn5uqKz90JfdB8NI06Z4o4WyoOyOPPmHfJo2ud5TvMVWgW4lVAhnKOaplEzJ70_3CH4Xs59j9jVmv4vZb6vmw954cz9Q96L4k2sFxAyUOhofKP_d_D_Xj7MohcmHh9wXf_dDAEpAB0Y7lL8B-oGRlA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>815406530</pqid></control><display><type>article</type><title>p-AKT overexpression in primary renal cell carcinomas and their metastases</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Hager, Martina ; Haufe, Heike ; Lusuardi, Lukas ; Schmeller, Nikolaus ; Kolbitsch, Christian</creator><creatorcontrib>Hager, Martina ; Haufe, Heike ; Lusuardi, Lukas ; Schmeller, Nikolaus ; Kolbitsch, Christian</creatorcontrib><description>In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluated p-AKT expression in a tissue microarray of primary renal cell carcinomas (PRCCs) (n = 45), their metastases (primary onset n = 45, secondary onset n = 5), and normal renal parenchyma (n = 45) by means of immunohistochemistry. Total p-AKT overexpression was found in 24/45 (53.3%) PRCCs, in 32/45 (71.1%) primary and in 3/5 (60%) secondary onset metastases. Membranous p-AKT overexpression was seen more frequently in PRCCs, namely 11/45 (24.4%), than in primary onset metastases 1/45 (2.2%). Overexpression of total p-AKT solely in metastases without overexpression in PRCC was exclusively demonstrated in primary onset metastases, namely in 28.9%. Patients with total p-AKT overexpression in primary carcinomas showed a trend to longer, and those with total p-AKT overexpression in metastases a tendency to shorter survival. In conclusion, the present study shows total p-AKT overexpression to be more frequent in metastases than in PRCCs. Total p-AKT overexpression in metastases without concomitant overexpression in their primary tumors was found in approximately one-third of primary onset metastases, which is interesting with regard to the association between high p-AKT expression and sensitivity to mTOR inhibitor therapy.</description><identifier>ISSN: 0262-0898</identifier><identifier>EISSN: 1573-7276</identifier><identifier>DOI: 10.1007/s10585-010-9351-y</identifier><identifier>PMID: 20844931</identifier><identifier>CODEN: CEXMD2</identifier><language>eng</language><publisher>Dordrecht: Dordrecht : Springer Netherlands</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - pathology ; Female ; Hematology ; Humans ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Male ; metastasis ; Middle Aged ; Neoplasm Metastasis - genetics ; Neoplasm Staging ; Oncology ; Overexpression ; p-AKT ; Proto-Oncogene Proteins c-akt - biosynthesis ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Renal cell carcinoma ; Research Paper ; Surgical Oncology</subject><ispartof>Clinical & experimental metastasis, 2010-12, Vol.27 (8), p.611-617</ispartof><rights>Springer Science+Business Media B.V. 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-32c5f61d1f77df04ff70c43dd76ce0f5f626d4c69ea5eed31f18a8196cb690f73</citedby><cites>FETCH-LOGICAL-c394t-32c5f61d1f77df04ff70c43dd76ce0f5f626d4c69ea5eed31f18a8196cb690f73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10585-010-9351-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10585-010-9351-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20844931$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hager, Martina</creatorcontrib><creatorcontrib>Haufe, Heike</creatorcontrib><creatorcontrib>Lusuardi, Lukas</creatorcontrib><creatorcontrib>Schmeller, Nikolaus</creatorcontrib><creatorcontrib>Kolbitsch, Christian</creatorcontrib><title>p-AKT overexpression in primary renal cell carcinomas and their metastases</title><title>Clinical & experimental metastasis</title><addtitle>Clin Exp Metastasis</addtitle><addtitle>Clin Exp Metastasis</addtitle><description>In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluated p-AKT expression in a tissue microarray of primary renal cell carcinomas (PRCCs) (n = 45), their metastases (primary onset n = 45, secondary onset n = 5), and normal renal parenchyma (n = 45) by means of immunohistochemistry. Total p-AKT overexpression was found in 24/45 (53.3%) PRCCs, in 32/45 (71.1%) primary and in 3/5 (60%) secondary onset metastases. Membranous p-AKT overexpression was seen more frequently in PRCCs, namely 11/45 (24.4%), than in primary onset metastases 1/45 (2.2%). Overexpression of total p-AKT solely in metastases without overexpression in PRCC was exclusively demonstrated in primary onset metastases, namely in 28.9%. Patients with total p-AKT overexpression in primary carcinomas showed a trend to longer, and those with total p-AKT overexpression in metastases a tendency to shorter survival. In conclusion, the present study shows total p-AKT overexpression to be more frequent in metastases than in PRCCs. Total p-AKT overexpression in metastases without concomitant overexpression in their primary tumors was found in approximately one-third of primary onset metastases, which is interesting with regard to the association between high p-AKT expression and sensitivity to mTOR inhibitor therapy.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Female</subject><subject>Hematology</subject><subject>Humans</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Male</subject><subject>metastasis</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>Overexpression</subject><subject>p-AKT</subject><subject>Proto-Oncogene Proteins c-akt - biosynthesis</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Renal cell carcinoma</subject><subject>Research Paper</subject><subject>Surgical Oncology</subject><issn>0262-0898</issn><issn>1573-7276</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kMtuFDEQRS0EIpPAB2QDrWyyMlTZbj-WUZQHEIkFydpy3OWko-nuwZ6JmL_Hox6CxAKp5FrUubdcl7FjhE8IYD4XhNa2HBC4ky3y7Su2wNZIboTRr9kChBYcrLMH7LCUJwBQxti37ECAVcpJXLCvK3727baZninTr1WmUvppbPqxWeV-CHnbZBrDsom0rE_IsR-nIZQmjF2zfqQ-NwOtQ6lF5R17k8Ky0Pt9P2J3lxe359f85vvVl_OzGx6lU2suRWyTxg6TMV0ClZKBqGTXGR0JUp0J3amoHYWWqJOY0AaLTsd77SAZecROZ99Vnn5uqKz90JfdB8NI06Z4o4WyoOyOPPmHfJo2ud5TvMVWgW4lVAhnKOaplEzJ70_3CH4Xs59j9jVmv4vZb6vmw954cz9Q96L4k2sFxAyUOhofKP_d_D_Xj7MohcmHh9wXf_dDAEpAB0Y7lL8B-oGRlA</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>Hager, Martina</creator><creator>Haufe, Heike</creator><creator>Lusuardi, Lukas</creator><creator>Schmeller, Nikolaus</creator><creator>Kolbitsch, Christian</creator><general>Dordrecht : Springer Netherlands</general><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>FBQ</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20101201</creationdate><title>p-AKT overexpression in primary renal cell carcinomas and their metastases</title><author>Hager, Martina ; Haufe, Heike ; Lusuardi, Lukas ; Schmeller, Nikolaus ; Kolbitsch, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c394t-32c5f61d1f77df04ff70c43dd76ce0f5f626d4c69ea5eed31f18a8196cb690f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Female</topic><topic>Hematology</topic><topic>Humans</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Male</topic><topic>metastasis</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>Overexpression</topic><topic>p-AKT</topic><topic>Proto-Oncogene Proteins c-akt - biosynthesis</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Renal cell carcinoma</topic><topic>Research Paper</topic><topic>Surgical Oncology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hager, Martina</creatorcontrib><creatorcontrib>Haufe, Heike</creatorcontrib><creatorcontrib>Lusuardi, Lukas</creatorcontrib><creatorcontrib>Schmeller, Nikolaus</creatorcontrib><creatorcontrib>Kolbitsch, Christian</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical & experimental metastasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hager, Martina</au><au>Haufe, Heike</au><au>Lusuardi, Lukas</au><au>Schmeller, Nikolaus</au><au>Kolbitsch, Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p-AKT overexpression in primary renal cell carcinomas and their metastases</atitle><jtitle>Clinical & experimental metastasis</jtitle><stitle>Clin Exp Metastasis</stitle><addtitle>Clin Exp Metastasis</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>27</volume><issue>8</issue><spage>611</spage><epage>617</epage><pages>611-617</pages><issn>0262-0898</issn><eissn>1573-7276</eissn><coden>CEXMD2</coden><abstract>In cancer therapy novel concepts focus on phosphoinositide 3-kinase (PI3K)/activated protein kinase B (p-AKT)/mammalian target of rapamycin (mTOR) inhibitors. In this context, p-AKT overexpression was previously shown to be associated with sensitivity to inhibitors of mTOR. The present study evaluated p-AKT expression in a tissue microarray of primary renal cell carcinomas (PRCCs) (n = 45), their metastases (primary onset n = 45, secondary onset n = 5), and normal renal parenchyma (n = 45) by means of immunohistochemistry. Total p-AKT overexpression was found in 24/45 (53.3%) PRCCs, in 32/45 (71.1%) primary and in 3/5 (60%) secondary onset metastases. Membranous p-AKT overexpression was seen more frequently in PRCCs, namely 11/45 (24.4%), than in primary onset metastases 1/45 (2.2%). Overexpression of total p-AKT solely in metastases without overexpression in PRCC was exclusively demonstrated in primary onset metastases, namely in 28.9%. Patients with total p-AKT overexpression in primary carcinomas showed a trend to longer, and those with total p-AKT overexpression in metastases a tendency to shorter survival. In conclusion, the present study shows total p-AKT overexpression to be more frequent in metastases than in PRCCs. Total p-AKT overexpression in metastases without concomitant overexpression in their primary tumors was found in approximately one-third of primary onset metastases, which is interesting with regard to the association between high p-AKT expression and sensitivity to mTOR inhibitor therapy.</abstract><cop>Dordrecht</cop><pub>Dordrecht : Springer Netherlands</pub><pmid>20844931</pmid><doi>10.1007/s10585-010-9351-y</doi><tpages>7</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0262-0898 |
ispartof | Clinical & experimental metastasis, 2010-12, Vol.27 (8), p.611-617 |
issn | 0262-0898 1573-7276 |
language | eng |
recordid | cdi_proquest_miscellaneous_762480487 |
source | MEDLINE; SpringerNature Journals |
subjects | Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - pathology Female Hematology Humans Kidney Neoplasms - genetics Kidney Neoplasms - pathology Male metastasis Middle Aged Neoplasm Metastasis - genetics Neoplasm Staging Oncology Overexpression p-AKT Proto-Oncogene Proteins c-akt - biosynthesis Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Renal cell carcinoma Research Paper Surgical Oncology |
title | p-AKT overexpression in primary renal cell carcinomas and their metastases |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T14%3A44%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=p-AKT%20overexpression%20in%20primary%20renal%20cell%20carcinomas%20and%20their%20metastases&rft.jtitle=Clinical%20&%20experimental%20metastasis&rft.au=Hager,%20Martina&rft.date=2010-12-01&rft.volume=27&rft.issue=8&rft.spage=611&rft.epage=617&rft.pages=611-617&rft.issn=0262-0898&rft.eissn=1573-7276&rft.coden=CEXMD2&rft_id=info:doi/10.1007/s10585-010-9351-y&rft_dat=%3Cproquest_cross%3E2202699771%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=815406530&rft_id=info:pmid/20844931&rfr_iscdi=true |