Effects of the estrogen receptor antagonist fulvestrant on F344 rat prolactinoma models
The relationship between estrogen and prolactinoma is well documented. But the anti-tumor effects of a pure estrogen receptor antagonist fulvestrant on prolactinomas, especially in vivo, and the possible mechanisms are still unclear. Therefore, the aim of this study was to evaluate the effects of fu...
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| Veröffentlicht in: | Journal of neuro-oncology 2014-02, Vol.116 (3), p.523-531 |
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| creator | Cao, Lei Gao, Hua Gui, Songbai Bai, Giwei Lu, Runchun Wang, Fei Zhang, Yazhuo |
| description | The relationship between estrogen and prolactinoma is well documented. But the anti-tumor effects of a pure estrogen receptor antagonist fulvestrant on prolactinomas, especially in vivo, and the possible mechanisms are still unclear. Therefore, the aim of this study was to evaluate the effects of fulvestrant and the involvement of the Wnt signaling pathway on rat prolactinoma models. Forty female F344 rat prolactinoma models were established by subcutaneous administration of 10 mg 17β-estradiol for 6 weeks. Rats were intramuscularly injected with fulvestrant (0, 0.5, 3, 20, 40 mg/kg), and tumor size, weight and serum prolactin (PRL) levels were evaluated before and after fulvestrant treatment at 3, 7 and 14 days. Expression of estrogen receptor α (ERα), β-catenin and Wnt inhibitory factor-1 (WIF-1) in prolactinomas was measured using quantitative PCR and western blotting, and methylation of the WIF-1 promoter was investigated using pyrosequencing. Tumor size, weight and serum PRL levels were inhibited in dose-dependent and time-dependent manners after fulvestrant treatments. β-catenin expression was downregulated but WIF-1 expression was upregulated following fulvestrant treatment. The methylation of the CpG site of the WIF-1 promoter was negatively correlated to the expression of WIF-1. In addition, the anti-cell proliferation of fulvestrant on GH3 cells was partly disrupted by Wnt signaling pathway agonist SB 216763. In conclusion, fulvestrant inhibited tumor proliferation and PRL secretion of prolactinomas via ERα, and the Wnt signaling pathway was involved in this anti-tumor effect. Therefore, fulvestrant may be a potential new drug for prolactinomas. |
| doi_str_mv | 10.1007/s11060-013-1351-8 |
| format | Article |
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But the anti-tumor effects of a pure estrogen receptor antagonist fulvestrant on prolactinomas, especially in vivo, and the possible mechanisms are still unclear. Therefore, the aim of this study was to evaluate the effects of fulvestrant and the involvement of the Wnt signaling pathway on rat prolactinoma models. Forty female F344 rat prolactinoma models were established by subcutaneous administration of 10 mg 17β-estradiol for 6 weeks. Rats were intramuscularly injected with fulvestrant (0, 0.5, 3, 20, 40 mg/kg), and tumor size, weight and serum prolactin (PRL) levels were evaluated before and after fulvestrant treatment at 3, 7 and 14 days. Expression of estrogen receptor α (ERα), β-catenin and Wnt inhibitory factor-1 (WIF-1) in prolactinomas was measured using quantitative PCR and western blotting, and methylation of the WIF-1 promoter was investigated using pyrosequencing. Tumor size, weight and serum PRL levels were inhibited in dose-dependent and time-dependent manners after fulvestrant treatments. β-catenin expression was downregulated but WIF-1 expression was upregulated following fulvestrant treatment. The methylation of the CpG site of the WIF-1 promoter was negatively correlated to the expression of WIF-1. In addition, the anti-cell proliferation of fulvestrant on GH3 cells was partly disrupted by Wnt signaling pathway agonist SB 216763. In conclusion, fulvestrant inhibited tumor proliferation and PRL secretion of prolactinomas via ERα, and the Wnt signaling pathway was involved in this anti-tumor effect. Therefore, fulvestrant may be a potential new drug for prolactinomas.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/s11060-013-1351-8</identifier><identifier>PMID: 24407733</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>17 beta -Estradiol ; Animals ; Cell Line, Transformed ; Disease Models, Animal ; DNA Methylation - drug effects ; Dose-Response Relationship, Drug ; Enzyme Inhibitors - pharmacology ; Estradiol - administration & dosage ; Estradiol - analogs & derivatives ; Estradiol - therapeutic use ; Estrogen Antagonists - therapeutic use ; Estrogen Receptor alpha - genetics ; Estrogen Receptor alpha - metabolism ; Estrogens - administration & dosage ; Extracellular Matrix Proteins - genetics ; Extracellular Matrix Proteins - metabolism ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Indoles - pharmacology ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Laboratory Investigation ; Maleimides - pharmacology ; Medicine ; Medicine & Public Health ; Neurology ; Oncology ; Pituitary Neoplasms - blood ; Pituitary Neoplasms - drug therapy ; Prolactin - blood ; Prolactinoma - blood ; Prolactinoma - drug therapy ; Rats ; Rats, Inbred F344 ; Time Factors</subject><ispartof>Journal of neuro-oncology, 2014-02, Vol.116 (3), p.523-531</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-1b73555a404ba7794b67d3e0ff4aa1111a5c1efdb30e6c222b1d685fb51ea5133</citedby><cites>FETCH-LOGICAL-c471t-1b73555a404ba7794b67d3e0ff4aa1111a5c1efdb30e6c222b1d685fb51ea5133</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/s11060-013-1351-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11060-013-1351-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24407733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cao, Lei</creatorcontrib><creatorcontrib>Gao, Hua</creatorcontrib><creatorcontrib>Gui, Songbai</creatorcontrib><creatorcontrib>Bai, Giwei</creatorcontrib><creatorcontrib>Lu, Runchun</creatorcontrib><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Zhang, Yazhuo</creatorcontrib><title>Effects of the estrogen receptor antagonist fulvestrant on F344 rat prolactinoma models</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><addtitle>J Neurooncol</addtitle><description>The relationship between estrogen and prolactinoma is well documented. But the anti-tumor effects of a pure estrogen receptor antagonist fulvestrant on prolactinomas, especially in vivo, and the possible mechanisms are still unclear. Therefore, the aim of this study was to evaluate the effects of fulvestrant and the involvement of the Wnt signaling pathway on rat prolactinoma models. Forty female F344 rat prolactinoma models were established by subcutaneous administration of 10 mg 17β-estradiol for 6 weeks. Rats were intramuscularly injected with fulvestrant (0, 0.5, 3, 20, 40 mg/kg), and tumor size, weight and serum prolactin (PRL) levels were evaluated before and after fulvestrant treatment at 3, 7 and 14 days. Expression of estrogen receptor α (ERα), β-catenin and Wnt inhibitory factor-1 (WIF-1) in prolactinomas was measured using quantitative PCR and western blotting, and methylation of the WIF-1 promoter was investigated using pyrosequencing. Tumor size, weight and serum PRL levels were inhibited in dose-dependent and time-dependent manners after fulvestrant treatments. β-catenin expression was downregulated but WIF-1 expression was upregulated following fulvestrant treatment. The methylation of the CpG site of the WIF-1 promoter was negatively correlated to the expression of WIF-1. In addition, the anti-cell proliferation of fulvestrant on GH3 cells was partly disrupted by Wnt signaling pathway agonist SB 216763. In conclusion, fulvestrant inhibited tumor proliferation and PRL secretion of prolactinomas via ERα, and the Wnt signaling pathway was involved in this anti-tumor effect. Therefore, fulvestrant may be a potential new drug for prolactinomas.</description><subject>17 beta -Estradiol</subject><subject>Animals</subject><subject>Cell Line, Transformed</subject><subject>Disease Models, Animal</subject><subject>DNA Methylation - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Estradiol - administration & dosage</subject><subject>Estradiol - analogs & derivatives</subject><subject>Estradiol - therapeutic use</subject><subject>Estrogen Antagonists - therapeutic use</subject><subject>Estrogen Receptor alpha - genetics</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogens - administration & dosage</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Indoles - pharmacology</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Laboratory Investigation</subject><subject>Maleimides - pharmacology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Pituitary Neoplasms - blood</subject><subject>Pituitary Neoplasms - drug therapy</subject><subject>Prolactin - blood</subject><subject>Prolactinoma - blood</subject><subject>Prolactinoma - drug therapy</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Time Factors</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kE1LAzEURYMotn78ADcScONmNG-STKZLKfUDCm4U3YXMzEttmZnUJCP4701pFRHMJpCcd9_lEHIG7AoYU9cBgBUsY8Az4BKyco-MQSqeKa74PhkzKFQmJ-J1RI5CWDHGhOJwSEa5EEwpzsfkZWYt1jFQZ2l8Q4oherfAnnqscR2dp6aPZuH6ZYjUDu3HBkhP1PX0lgtBvYl07V1r6rjsXWdo5xpswwk5sKYNeLq7j8nz7expep_NH-8epjfzrBYKYgaV4lJKI5iojFITURWq4cisFcZAOkbWgLapOMOizvO8gqYopa0koJHA-TG53OamDu9DKqe7ZaixbU2PbggaZBKloCxYQi_-oCs3-D610yAmeQ5lPlGJgi1VexeCR6vXftkZ_6mB6Y11vbWuk3W9sa7LNHO-Sx6qDpufiW_NCci3QEhf_QL9r9X_pn4BMjOMJA</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Cao, Lei</creator><creator>Gao, Hua</creator><creator>Gui, Songbai</creator><creator>Bai, Giwei</creator><creator>Lu, Runchun</creator><creator>Wang, Fei</creator><creator>Zhang, Yazhuo</creator><general>Springer US</general><general>Springer Nature B.V</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20140201</creationdate><title>Effects of the estrogen receptor antagonist fulvestrant on F344 rat prolactinoma models</title><author>Cao, Lei ; Gao, Hua ; Gui, Songbai ; Bai, Giwei ; Lu, Runchun ; Wang, Fei ; Zhang, Yazhuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-1b73555a404ba7794b67d3e0ff4aa1111a5c1efdb30e6c222b1d685fb51ea5133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>17 beta -Estradiol</topic><topic>Animals</topic><topic>Cell Line, Transformed</topic><topic>Disease Models, Animal</topic><topic>DNA Methylation - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Estradiol - administration & dosage</topic><topic>Estradiol - analogs & derivatives</topic><topic>Estradiol - therapeutic use</topic><topic>Estrogen Antagonists - therapeutic use</topic><topic>Estrogen Receptor alpha - genetics</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogens - administration & dosage</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Indoles - pharmacology</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Laboratory Investigation</topic><topic>Maleimides - pharmacology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Pituitary Neoplasms - blood</topic><topic>Pituitary Neoplasms - drug therapy</topic><topic>Prolactin - blood</topic><topic>Prolactinoma - blood</topic><topic>Prolactinoma - drug therapy</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Lei</creatorcontrib><creatorcontrib>Gao, Hua</creatorcontrib><creatorcontrib>Gui, Songbai</creatorcontrib><creatorcontrib>Bai, Giwei</creatorcontrib><creatorcontrib>Lu, Runchun</creatorcontrib><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Zhang, Yazhuo</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>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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</collection><collection>ProQuest One Community College</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>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><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cao, Lei</au><au>Gao, Hua</au><au>Gui, Songbai</au><au>Bai, Giwei</au><au>Lu, Runchun</au><au>Wang, Fei</au><au>Zhang, Yazhuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of the estrogen receptor antagonist fulvestrant on F344 rat prolactinoma models</atitle><jtitle>Journal of neuro-oncology</jtitle><stitle>J Neurooncol</stitle><addtitle>J Neurooncol</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>116</volume><issue>3</issue><spage>523</spage><epage>531</epage><pages>523-531</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><abstract>The relationship between estrogen and prolactinoma is well documented. But the anti-tumor effects of a pure estrogen receptor antagonist fulvestrant on prolactinomas, especially in vivo, and the possible mechanisms are still unclear. Therefore, the aim of this study was to evaluate the effects of fulvestrant and the involvement of the Wnt signaling pathway on rat prolactinoma models. Forty female F344 rat prolactinoma models were established by subcutaneous administration of 10 mg 17β-estradiol for 6 weeks. Rats were intramuscularly injected with fulvestrant (0, 0.5, 3, 20, 40 mg/kg), and tumor size, weight and serum prolactin (PRL) levels were evaluated before and after fulvestrant treatment at 3, 7 and 14 days. Expression of estrogen receptor α (ERα), β-catenin and Wnt inhibitory factor-1 (WIF-1) in prolactinomas was measured using quantitative PCR and western blotting, and methylation of the WIF-1 promoter was investigated using pyrosequencing. Tumor size, weight and serum PRL levels were inhibited in dose-dependent and time-dependent manners after fulvestrant treatments. β-catenin expression was downregulated but WIF-1 expression was upregulated following fulvestrant treatment. The methylation of the CpG site of the WIF-1 promoter was negatively correlated to the expression of WIF-1. In addition, the anti-cell proliferation of fulvestrant on GH3 cells was partly disrupted by Wnt signaling pathway agonist SB 216763. In conclusion, fulvestrant inhibited tumor proliferation and PRL secretion of prolactinomas via ERα, and the Wnt signaling pathway was involved in this anti-tumor effect. Therefore, fulvestrant may be a potential new drug for prolactinomas.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24407733</pmid><doi>10.1007/s11060-013-1351-8</doi><tpages>9</tpages></addata></record> |
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| subjects | 17 beta -Estradiol Animals Cell Line, Transformed Disease Models, Animal DNA Methylation - drug effects Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology Estradiol - administration & dosage Estradiol - analogs & derivatives Estradiol - therapeutic use Estrogen Antagonists - therapeutic use Estrogen Receptor alpha - genetics Estrogen Receptor alpha - metabolism Estrogens - administration & dosage Extracellular Matrix Proteins - genetics Extracellular Matrix Proteins - metabolism Female Gene Expression Regulation, Neoplastic - drug effects Indoles - pharmacology Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Laboratory Investigation Maleimides - pharmacology Medicine Medicine & Public Health Neurology Oncology Pituitary Neoplasms - blood Pituitary Neoplasms - drug therapy Prolactin - blood Prolactinoma - blood Prolactinoma - drug therapy Rats Rats, Inbred F344 Time Factors |
| title | Effects of the estrogen receptor antagonist fulvestrant on F344 rat prolactinoma models |
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