Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer
BACKGROUND: This study examined the clinical significance of CCNE1 (Cyclin E1) amplification and assessed whether CCNE1 is a potential therapeutic target in ovarian cancer. METHODS: CCNE1 expression and amplification in ovarian cancer was assessed by immunohistochemistry, fluorescence in situ hybrid...
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| Veröffentlicht in: | Cancer 2010-06, Vol.116 (11), p.2621-2634 |
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| creator | Nakayama, Naomi Nakayama, Kentaro Shamima, Yeasmin Ishikawa, Masako Katagiri, Atsuko Iida, Kouji Miyazaki, Khoji |
| description | BACKGROUND:
This study examined the clinical significance of CCNE1 (Cyclin E1) amplification and assessed whether CCNE1 is a potential therapeutic target in ovarian cancer.
METHODS:
CCNE1 expression and amplification in ovarian cancer was assessed by immunohistochemistry, fluorescence in situ hybridization and clinical data collected by retrospective chart review. CCNE1 gene knockdown using silencing RNA and a CCNE1 gene transfection system were used to asses CCNE1 function in tissue samples of ovarian cancer.
RESULTS:
Gene amplification was identified in 18 (20.4%) of 88 ovarian carcinomas. CCNE1 copy number significantly correlated with CCNE1 protein expression (r = 0.522, P < .0001). CCNE1 amplification significantly correlated with shorter disease‐free survival and overall survival (P < .001). There were nonsignificant trends between high protein expression and poor disease‐free survival (P = .2865) and overall survival (P = .1248). Multivariate analysis showed gene amplification was an independent prognostic factor for disease‐free survival and overall survival after standard platinum‐taxane chemotherapy (P = .0274, P = .0023). Profound growth inhibition and apoptosis were observed in silencing RNA‐treated cancer cells with gene amplification compared with results in cancer cells with CCNE1 moderate expression without gene amplification or with low CCNE1 expression. CCNE1 overexpression stimulated proliferation in ovarian cancer cell lines ES2 and TOV‐21G, which have lower endogenous CCNE1 expression.
CONCLUSIONS:
These findings indicate that CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. Furthermore, they suggest that CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers. Therefore, CCNE1‐targeted therapy may benefit ovarian cancer patients with CCNE1 amplification. Cancer 2010. © 2010 American Cancer Society.
CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers. |
| doi_str_mv | 10.1002/cncr.24987 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1238121758</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1238121758</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4617-35fa43f1149039caff1367d3c500ccb6411786a8af824104b99c07d12cbbd1eb3</originalsourceid><addsrcrecordid>eNp90EFrFDEUB_Agil2rFz-A5CKIMG1ektnJHGWoVSgtFAVvw5vMS43MZsYks9Jv39Rd9eYpvPDj_ZM_Y69BnIEQ8twGG8-kbk3zhG1AtE0lQMunbCOEMFWt1bcT9iKlH2VsZK2esxMplNo2Rm_Y3SUF4rhbJu-8xeznwLvu-gK4TzzShJlGnme-zHPkaY17v8eJYxjLTaaQfZnyd4q40Jq95RnjHWXuA5_3GD0GbjFYii_ZM4dTolfH85R9_XjxpftUXd1cfu4-XFVWb6GpVO1QKwegW6Fai85BeeiobC2EtcNWAzRmiwadkRqEHtrWimYEaYdhBBrUKXt32LvE-edKKfc7nyxNEwaa19SDVAYkNLUp9P2B2jinFMn1S_Q7jPc9iP6x2P6x2P53sQW_Oe5dhx2Nf-mfJgt4ewSYLE4ulm_79M9JU5Lbujg4uF9-ovv_RPbddXd7CH8AVXeQdg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1238121758</pqid></control><display><type>article</type><title>Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley Free Content</source><source>Alma/SFX Local Collection</source><creator>Nakayama, Naomi ; Nakayama, Kentaro ; Shamima, Yeasmin ; Ishikawa, Masako ; Katagiri, Atsuko ; Iida, Kouji ; Miyazaki, Khoji</creator><creatorcontrib>Nakayama, Naomi ; Nakayama, Kentaro ; Shamima, Yeasmin ; Ishikawa, Masako ; Katagiri, Atsuko ; Iida, Kouji ; Miyazaki, Khoji</creatorcontrib><description>BACKGROUND:
This study examined the clinical significance of CCNE1 (Cyclin E1) amplification and assessed whether CCNE1 is a potential therapeutic target in ovarian cancer.
METHODS:
CCNE1 expression and amplification in ovarian cancer was assessed by immunohistochemistry, fluorescence in situ hybridization and clinical data collected by retrospective chart review. CCNE1 gene knockdown using silencing RNA and a CCNE1 gene transfection system were used to asses CCNE1 function in tissue samples of ovarian cancer.
RESULTS:
Gene amplification was identified in 18 (20.4%) of 88 ovarian carcinomas. CCNE1 copy number significantly correlated with CCNE1 protein expression (r = 0.522, P < .0001). CCNE1 amplification significantly correlated with shorter disease‐free survival and overall survival (P < .001). There were nonsignificant trends between high protein expression and poor disease‐free survival (P = .2865) and overall survival (P = .1248). Multivariate analysis showed gene amplification was an independent prognostic factor for disease‐free survival and overall survival after standard platinum‐taxane chemotherapy (P = .0274, P = .0023). Profound growth inhibition and apoptosis were observed in silencing RNA‐treated cancer cells with gene amplification compared with results in cancer cells with CCNE1 moderate expression without gene amplification or with low CCNE1 expression. CCNE1 overexpression stimulated proliferation in ovarian cancer cell lines ES2 and TOV‐21G, which have lower endogenous CCNE1 expression.
CONCLUSIONS:
These findings indicate that CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. Furthermore, they suggest that CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers. Therefore, CCNE1‐targeted therapy may benefit ovarian cancer patients with CCNE1 amplification. Cancer 2010. © 2010 American Cancer Society.
CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers.</description><identifier>ISSN: 0008-543X</identifier><identifier>ISSN: 1097-0142</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/cncr.24987</identifier><identifier>PMID: 20336784</identifier><identifier>CODEN: CANCAR</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Apoptosis ; Biological and medical sciences ; CCNE1 ; Cell Line, Tumor ; Cell Proliferation ; Chemotherapy ; copy number ; Cyclin E - genetics ; Cyclin E - metabolism ; Cyclin E1 ; Cyclins ; Data processing ; Disease-Free Survival ; Female ; Female genital diseases ; Fluorescence in situ hybridization ; Gene Amplification ; Gene Dosage ; Gene Knockdown Techniques ; Gene silencing ; Gynecology. Andrology. Obstetrics ; Humans ; Immunohistochemistry ; Medical sciences ; Middle Aged ; Multivariate analysis ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Ovarian carcinoma ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - mortality ; RNA ; RNA-mediated interference ; Survival ; Transfection ; Tumor cell lines ; Tumors</subject><ispartof>Cancer, 2010-06, Vol.116 (11), p.2621-2634</ispartof><rights>Copyright © 2010 American Cancer Society</rights><rights>2015 INIST-CNRS</rights><rights>(c) 2010 American Cancer Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4617-35fa43f1149039caff1367d3c500ccb6411786a8af824104b99c07d12cbbd1eb3</citedby><cites>FETCH-LOGICAL-c4617-35fa43f1149039caff1367d3c500ccb6411786a8af824104b99c07d12cbbd1eb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcncr.24987$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcncr.24987$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,1430,27911,27912,45561,45562,46396,46820</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22823895$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20336784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakayama, Naomi</creatorcontrib><creatorcontrib>Nakayama, Kentaro</creatorcontrib><creatorcontrib>Shamima, Yeasmin</creatorcontrib><creatorcontrib>Ishikawa, Masako</creatorcontrib><creatorcontrib>Katagiri, Atsuko</creatorcontrib><creatorcontrib>Iida, Kouji</creatorcontrib><creatorcontrib>Miyazaki, Khoji</creatorcontrib><title>Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer</title><title>Cancer</title><addtitle>Cancer</addtitle><description>BACKGROUND:
This study examined the clinical significance of CCNE1 (Cyclin E1) amplification and assessed whether CCNE1 is a potential therapeutic target in ovarian cancer.
METHODS:
CCNE1 expression and amplification in ovarian cancer was assessed by immunohistochemistry, fluorescence in situ hybridization and clinical data collected by retrospective chart review. CCNE1 gene knockdown using silencing RNA and a CCNE1 gene transfection system were used to asses CCNE1 function in tissue samples of ovarian cancer.
RESULTS:
Gene amplification was identified in 18 (20.4%) of 88 ovarian carcinomas. CCNE1 copy number significantly correlated with CCNE1 protein expression (r = 0.522, P < .0001). CCNE1 amplification significantly correlated with shorter disease‐free survival and overall survival (P < .001). There were nonsignificant trends between high protein expression and poor disease‐free survival (P = .2865) and overall survival (P = .1248). Multivariate analysis showed gene amplification was an independent prognostic factor for disease‐free survival and overall survival after standard platinum‐taxane chemotherapy (P = .0274, P = .0023). Profound growth inhibition and apoptosis were observed in silencing RNA‐treated cancer cells with gene amplification compared with results in cancer cells with CCNE1 moderate expression without gene amplification or with low CCNE1 expression. CCNE1 overexpression stimulated proliferation in ovarian cancer cell lines ES2 and TOV‐21G, which have lower endogenous CCNE1 expression.
CONCLUSIONS:
These findings indicate that CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. Furthermore, they suggest that CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers. Therefore, CCNE1‐targeted therapy may benefit ovarian cancer patients with CCNE1 amplification. Cancer 2010. © 2010 American Cancer Society.
CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers.</description><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>CCNE1</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Chemotherapy</subject><subject>copy number</subject><subject>Cyclin E - genetics</subject><subject>Cyclin E - metabolism</subject><subject>Cyclin E1</subject><subject>Cyclins</subject><subject>Data processing</subject><subject>Disease-Free Survival</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Fluorescence in situ hybridization</subject><subject>Gene Amplification</subject><subject>Gene Dosage</subject><subject>Gene Knockdown Techniques</subject><subject>Gene silencing</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multivariate analysis</subject><subject>Oncogene Proteins - genetics</subject><subject>Oncogene Proteins - metabolism</subject><subject>Ovarian carcinoma</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - mortality</subject><subject>RNA</subject><subject>RNA-mediated interference</subject><subject>Survival</subject><subject>Transfection</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><issn>0008-543X</issn><issn>1097-0142</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90EFrFDEUB_Agil2rFz-A5CKIMG1ektnJHGWoVSgtFAVvw5vMS43MZsYks9Jv39Rd9eYpvPDj_ZM_Y69BnIEQ8twGG8-kbk3zhG1AtE0lQMunbCOEMFWt1bcT9iKlH2VsZK2esxMplNo2Rm_Y3SUF4rhbJu-8xeznwLvu-gK4TzzShJlGnme-zHPkaY17v8eJYxjLTaaQfZnyd4q40Jq95RnjHWXuA5_3GD0GbjFYii_ZM4dTolfH85R9_XjxpftUXd1cfu4-XFVWb6GpVO1QKwegW6Fai85BeeiobC2EtcNWAzRmiwadkRqEHtrWimYEaYdhBBrUKXt32LvE-edKKfc7nyxNEwaa19SDVAYkNLUp9P2B2jinFMn1S_Q7jPc9iP6x2P6x2P53sQW_Oe5dhx2Nf-mfJgt4ewSYLE4ulm_79M9JU5Lbujg4uF9-ovv_RPbddXd7CH8AVXeQdg</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Nakayama, Naomi</creator><creator>Nakayama, Kentaro</creator><creator>Shamima, Yeasmin</creator><creator>Ishikawa, Masako</creator><creator>Katagiri, Atsuko</creator><creator>Iida, Kouji</creator><creator>Miyazaki, Khoji</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Blackwell</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20100601</creationdate><title>Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer</title><author>Nakayama, Naomi ; Nakayama, Kentaro ; Shamima, Yeasmin ; Ishikawa, Masako ; Katagiri, Atsuko ; Iida, Kouji ; Miyazaki, Khoji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4617-35fa43f1149039caff1367d3c500ccb6411786a8af824104b99c07d12cbbd1eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>CCNE1</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Chemotherapy</topic><topic>copy number</topic><topic>Cyclin E - genetics</topic><topic>Cyclin E - metabolism</topic><topic>Cyclin E1</topic><topic>Cyclins</topic><topic>Data processing</topic><topic>Disease-Free Survival</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Fluorescence in situ hybridization</topic><topic>Gene Amplification</topic><topic>Gene Dosage</topic><topic>Gene Knockdown Techniques</topic><topic>Gene silencing</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multivariate analysis</topic><topic>Oncogene Proteins - genetics</topic><topic>Oncogene Proteins - metabolism</topic><topic>Ovarian carcinoma</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - mortality</topic><topic>RNA</topic><topic>RNA-mediated interference</topic><topic>Survival</topic><topic>Transfection</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakayama, Naomi</creatorcontrib><creatorcontrib>Nakayama, Kentaro</creatorcontrib><creatorcontrib>Shamima, Yeasmin</creatorcontrib><creatorcontrib>Ishikawa, Masako</creatorcontrib><creatorcontrib>Katagiri, Atsuko</creatorcontrib><creatorcontrib>Iida, Kouji</creatorcontrib><creatorcontrib>Miyazaki, Khoji</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakayama, Naomi</au><au>Nakayama, Kentaro</au><au>Shamima, Yeasmin</au><au>Ishikawa, Masako</au><au>Katagiri, Atsuko</au><au>Iida, Kouji</au><au>Miyazaki, Khoji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>116</volume><issue>11</issue><spage>2621</spage><epage>2634</epage><pages>2621-2634</pages><issn>0008-543X</issn><issn>1097-0142</issn><eissn>1097-0142</eissn><coden>CANCAR</coden><abstract>BACKGROUND:
This study examined the clinical significance of CCNE1 (Cyclin E1) amplification and assessed whether CCNE1 is a potential therapeutic target in ovarian cancer.
METHODS:
CCNE1 expression and amplification in ovarian cancer was assessed by immunohistochemistry, fluorescence in situ hybridization and clinical data collected by retrospective chart review. CCNE1 gene knockdown using silencing RNA and a CCNE1 gene transfection system were used to asses CCNE1 function in tissue samples of ovarian cancer.
RESULTS:
Gene amplification was identified in 18 (20.4%) of 88 ovarian carcinomas. CCNE1 copy number significantly correlated with CCNE1 protein expression (r = 0.522, P < .0001). CCNE1 amplification significantly correlated with shorter disease‐free survival and overall survival (P < .001). There were nonsignificant trends between high protein expression and poor disease‐free survival (P = .2865) and overall survival (P = .1248). Multivariate analysis showed gene amplification was an independent prognostic factor for disease‐free survival and overall survival after standard platinum‐taxane chemotherapy (P = .0274, P = .0023). Profound growth inhibition and apoptosis were observed in silencing RNA‐treated cancer cells with gene amplification compared with results in cancer cells with CCNE1 moderate expression without gene amplification or with low CCNE1 expression. CCNE1 overexpression stimulated proliferation in ovarian cancer cell lines ES2 and TOV‐21G, which have lower endogenous CCNE1 expression.
CONCLUSIONS:
These findings indicate that CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. Furthermore, they suggest that CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers. Therefore, CCNE1‐targeted therapy may benefit ovarian cancer patients with CCNE1 amplification. Cancer 2010. © 2010 American Cancer Society.
CCNE1 overexpression is critical to growth and survival of ovarian cancer tumors with CCNE1 gene amplification. CCNE1 silencing RNA‐induced phenotypes depend on amplification status of ovarian cancers.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20336784</pmid><doi>10.1002/cncr.24987</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Biological and medical sciences CCNE1 Cell Line, Tumor Cell Proliferation Chemotherapy copy number Cyclin E - genetics Cyclin E - metabolism Cyclin E1 Cyclins Data processing Disease-Free Survival Female Female genital diseases Fluorescence in situ hybridization Gene Amplification Gene Dosage Gene Knockdown Techniques Gene silencing Gynecology. Andrology. Obstetrics Humans Immunohistochemistry Medical sciences Middle Aged Multivariate analysis Oncogene Proteins - genetics Oncogene Proteins - metabolism Ovarian carcinoma Ovarian Neoplasms - genetics Ovarian Neoplasms - mortality RNA RNA-mediated interference Survival Transfection Tumor cell lines Tumors |
| title | Gene amplification CCNE1 is related to poor survival and potential therapeutic target in ovarian cancer |
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