ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma
Activating transcription factor 2 (ATF2) is a basic helix-loop-helix transcription factor, which has been shown to participate in the pathobiology of numerous cancers. However, the role of ATF2 in renal cell carcinoma (RCC) remains unclear. ATF2 knockdown and overexpression studies were performed in...
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| Veröffentlicht in: | Journal of experimental & clinical cancer research 2016-07, Vol.35 (1), p.108-108, Article 108 |
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| container_title | Journal of experimental & clinical cancer research |
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| creator | Wu, Deng-Shuang Chen, Cheng Wu, Zhen-Jie Liu, Bing Gao, Li Yang, Qing Chen, Wei Chen, Jun-Ming Bao, Yi Qu, Le Wang, Lin-Hui |
| description | Activating transcription factor 2 (ATF2) is a basic helix-loop-helix transcription factor, which has been shown to participate in the pathobiology of numerous cancers. However, the role of ATF2 in renal cell carcinoma (RCC) remains unclear.
ATF2 knockdown and overexpression studies were performed in RCC cells to evaluate changes in cell viability, cell cycle, apoptosis, migration and invasion. Xenograft models were used to examine the tumorigenic and metastatic capability of RCC cells upon ATF2 suppression. The expression of ATF2 in human RCC samples was determined using immunohistochemistry on a tissue microarray.
ATF2 knockdown in RCC cells reduced their proliferative and metastatic potentials, whereas ATF2 overexpression enhanced these properties. Mechanistic studies revealed that the transcription of CyclinB1, CyclinD1, Snail and Vimentin was directly regulated by ATF2 in RCC cells. Moreover, ATF2 was shown to be highly expressed in RCC tissues, especially in tumors with metastases. High expression of ATF2 correlated with aggressive clinico-pathological characteristics and predicted poor prognosis of RCC patients.
ATF2 exerts an oncogenic role in RCC and could serve as an important prognostic biomarker. |
| doi_str_mv | 10.1186/s13046-016-0383-2 |
| format | Article |
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ATF2 knockdown and overexpression studies were performed in RCC cells to evaluate changes in cell viability, cell cycle, apoptosis, migration and invasion. Xenograft models were used to examine the tumorigenic and metastatic capability of RCC cells upon ATF2 suppression. The expression of ATF2 in human RCC samples was determined using immunohistochemistry on a tissue microarray.
ATF2 knockdown in RCC cells reduced their proliferative and metastatic potentials, whereas ATF2 overexpression enhanced these properties. Mechanistic studies revealed that the transcription of CyclinB1, CyclinD1, Snail and Vimentin was directly regulated by ATF2 in RCC cells. Moreover, ATF2 was shown to be highly expressed in RCC tissues, especially in tumors with metastases. High expression of ATF2 correlated with aggressive clinico-pathological characteristics and predicted poor prognosis of RCC patients.
ATF2 exerts an oncogenic role in RCC and could serve as an important prognostic biomarker.</description><identifier>ISSN: 1756-9966</identifier><identifier>ISSN: 0392-9078</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-016-0383-2</identifier><identifier>PMID: 27377902</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Activating Transcription Factor 2 - genetics ; Activating Transcription Factor 2 - metabolism ; Analysis ; Animals ; Apoptosis ; Carcinoma, Renal cell ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cell Survival ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genetic aspects ; Humans ; Immunohistochemistry ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Male ; Metastasis ; Mice ; Neoplasm Transplantation ; Prognosis ; Risk factors ; Tissue Array Analysis ; Up-Regulation</subject><ispartof>Journal of experimental & clinical cancer research, 2016-07, Vol.35 (1), p.108-108, Article 108</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-baf206738d6ed2d9989814de0f95b8b5242f03ea4535bb7e82c12b549dfbfd463</citedby><cites>FETCH-LOGICAL-c525t-baf206738d6ed2d9989814de0f95b8b5242f03ea4535bb7e82c12b549dfbfd463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932740/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932740/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27377902$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Deng-Shuang</creatorcontrib><creatorcontrib>Chen, Cheng</creatorcontrib><creatorcontrib>Wu, Zhen-Jie</creatorcontrib><creatorcontrib>Liu, Bing</creatorcontrib><creatorcontrib>Gao, Li</creatorcontrib><creatorcontrib>Yang, Qing</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Chen, Jun-Ming</creatorcontrib><creatorcontrib>Bao, Yi</creatorcontrib><creatorcontrib>Qu, Le</creatorcontrib><creatorcontrib>Wang, Lin-Hui</creatorcontrib><title>ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Activating transcription factor 2 (ATF2) is a basic helix-loop-helix transcription factor, which has been shown to participate in the pathobiology of numerous cancers. However, the role of ATF2 in renal cell carcinoma (RCC) remains unclear.
ATF2 knockdown and overexpression studies were performed in RCC cells to evaluate changes in cell viability, cell cycle, apoptosis, migration and invasion. Xenograft models were used to examine the tumorigenic and metastatic capability of RCC cells upon ATF2 suppression. The expression of ATF2 in human RCC samples was determined using immunohistochemistry on a tissue microarray.
ATF2 knockdown in RCC cells reduced their proliferative and metastatic potentials, whereas ATF2 overexpression enhanced these properties. Mechanistic studies revealed that the transcription of CyclinB1, CyclinD1, Snail and Vimentin was directly regulated by ATF2 in RCC cells. Moreover, ATF2 was shown to be highly expressed in RCC tissues, especially in tumors with metastases. High expression of ATF2 correlated with aggressive clinico-pathological characteristics and predicted poor prognosis of RCC patients.
ATF2 exerts an oncogenic role in RCC and could serve as an important prognostic biomarker.</description><subject>Activating Transcription Factor 2 - genetics</subject><subject>Activating Transcription Factor 2 - metabolism</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Carcinoma, Renal cell</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Knockdown Techniques</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Male</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Neoplasm Transplantation</subject><subject>Prognosis</subject><subject>Risk factors</subject><subject>Tissue Array Analysis</subject><subject>Up-Regulation</subject><issn>1756-9966</issn><issn>0392-9078</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkkuLFDEQx4Mo7kM_gBdpEMRLr3l35yIMi7sKC15WryHdqZ7J0p20SVrYb2_aWYcZkZBHJb-qVBV_hN4QfEVIKz8mwjCXNSZlspbV9Bk6J42QtVJSPj86n6GLlB4wlkQR9RKd0YY1jcL0HP3Y3N_Qao5gXZ9TNYcQixW2PiSXKuPtak0hQ6omM7qtNz5X8w58yI9zuXS-iuDNWPUwlsXE3vkwmVfoxWDGBK-f9kv0_ebz_fWX-u7b7dfrzV3dCypy3ZmBYtmw1kqw1CrVqpZwC3hQoms7QTkdMAPDBRNd10BLe0I7wZUdusFyyS7Rp33ceekmsD34HM2o5-gmEx91ME6fvni309vwS3PFaMNxCfDhKUAMPxdIWU8urbUYD2FJmrS4cLTkVdB3_6APYYml9j9Uo5jAJc8DtTUjaOeHUP7t16B6w6WiLVdCFerqP1QZFibXBw-DK_cnDu-PHHZgxrxLYVyyCz6dgmQP9jGkFGE4NINgvapG71Wji2r0qhpNi8_b4y4ePP7KhP0Ggvq8Tw</recordid><startdate>20160704</startdate><enddate>20160704</enddate><creator>Wu, Deng-Shuang</creator><creator>Chen, Cheng</creator><creator>Wu, Zhen-Jie</creator><creator>Liu, Bing</creator><creator>Gao, Li</creator><creator>Yang, Qing</creator><creator>Chen, Wei</creator><creator>Chen, Jun-Ming</creator><creator>Bao, Yi</creator><creator>Qu, Le</creator><creator>Wang, Lin-Hui</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160704</creationdate><title>ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma</title><author>Wu, Deng-Shuang ; Chen, Cheng ; Wu, Zhen-Jie ; Liu, Bing ; Gao, Li ; Yang, Qing ; Chen, Wei ; Chen, Jun-Ming ; Bao, Yi ; Qu, Le ; Wang, Lin-Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-baf206738d6ed2d9989814de0f95b8b5242f03ea4535bb7e82c12b549dfbfd463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Activating Transcription Factor 2 - genetics</topic><topic>Activating Transcription Factor 2 - metabolism</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Carcinoma, Renal cell</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Knockdown Techniques</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Male</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Neoplasm Transplantation</topic><topic>Prognosis</topic><topic>Risk factors</topic><topic>Tissue Array Analysis</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Deng-Shuang</creatorcontrib><creatorcontrib>Chen, Cheng</creatorcontrib><creatorcontrib>Wu, Zhen-Jie</creatorcontrib><creatorcontrib>Liu, Bing</creatorcontrib><creatorcontrib>Gao, Li</creatorcontrib><creatorcontrib>Yang, Qing</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Chen, Jun-Ming</creatorcontrib><creatorcontrib>Bao, Yi</creatorcontrib><creatorcontrib>Qu, Le</creatorcontrib><creatorcontrib>Wang, Lin-Hui</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central Essentials</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of experimental & clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Deng-Shuang</au><au>Chen, Cheng</au><au>Wu, Zhen-Jie</au><au>Liu, Bing</au><au>Gao, Li</au><au>Yang, Qing</au><au>Chen, Wei</au><au>Chen, Jun-Ming</au><au>Bao, Yi</au><au>Qu, Le</au><au>Wang, Lin-Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma</atitle><jtitle>Journal of experimental & clinical cancer research</jtitle><addtitle>J Exp Clin Cancer Res</addtitle><date>2016-07-04</date><risdate>2016</risdate><volume>35</volume><issue>1</issue><spage>108</spage><epage>108</epage><pages>108-108</pages><artnum>108</artnum><issn>1756-9966</issn><issn>0392-9078</issn><eissn>1756-9966</eissn><abstract>Activating transcription factor 2 (ATF2) is a basic helix-loop-helix transcription factor, which has been shown to participate in the pathobiology of numerous cancers. However, the role of ATF2 in renal cell carcinoma (RCC) remains unclear.
ATF2 knockdown and overexpression studies were performed in RCC cells to evaluate changes in cell viability, cell cycle, apoptosis, migration and invasion. Xenograft models were used to examine the tumorigenic and metastatic capability of RCC cells upon ATF2 suppression. The expression of ATF2 in human RCC samples was determined using immunohistochemistry on a tissue microarray.
ATF2 knockdown in RCC cells reduced their proliferative and metastatic potentials, whereas ATF2 overexpression enhanced these properties. Mechanistic studies revealed that the transcription of CyclinB1, CyclinD1, Snail and Vimentin was directly regulated by ATF2 in RCC cells. Moreover, ATF2 was shown to be highly expressed in RCC tissues, especially in tumors with metastases. High expression of ATF2 correlated with aggressive clinico-pathological characteristics and predicted poor prognosis of RCC patients.
ATF2 exerts an oncogenic role in RCC and could serve as an important prognostic biomarker.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27377902</pmid><doi>10.1186/s13046-016-0383-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Activating Transcription Factor 2 - genetics Activating Transcription Factor 2 - metabolism Analysis Animals Apoptosis Carcinoma, Renal cell Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology Cell Cycle Cell Line, Tumor Cell Movement Cell Proliferation Cell Survival Female Gene Expression Regulation, Neoplastic Gene Knockdown Techniques Genetic aspects Humans Immunohistochemistry Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Male Metastasis Mice Neoplasm Transplantation Prognosis Risk factors Tissue Array Analysis Up-Regulation |
| title | ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma |
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