Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma
DNA amplification is one of the mechanisms to activate genes that are implicated in neoplastic transformation and gain of chromosome band 3q26 is a common event in squamous cell carcinomas. The aim of the present work was to identify the specific target gene from four candidates (MDS1, PRKCI, ECT2,...
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Veröffentlicht in: | Genes chromosomes & cancer 2008-02, Vol.47 (2), p.127-136 |
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creator | Yang, Yi-Ling Chu, Jia-You Luo, Man-Li Wu, Yu-Peng Zhang, Yu Feng, Yan-Bin Shi, Zhi-Zhou Xu, Xin Han, Ya-Ling Cai, Yan Dong, Jin-Tang Zhan, Qi-Min Wu, Min Wang, Ming-Rong |
description | DNA amplification is one of the mechanisms to activate genes that are implicated in neoplastic transformation and gain of chromosome band 3q26 is a common event in squamous cell carcinomas. The aim of the present work was to identify the specific target gene from four candidates (MDS1, PRKCI, ECT2, and PIK3CA) located on 3q26 amplification in esophageal squamous cell carcinomas (ESCCs). To assess the prevalence of copy number gains of putative genes, fluorescence in situ hybridization (FISH) was applied on 108 ESCCs and 9 ESCC cell lines. Our data showed that MDS1 and PRKCI were more frequently gained. Positive correlation was found only for PRKCI between amplification and tumor size (P = 0.043), lymph node metastasis (P = 0.015) and clinical stage (P = 0.002). PRKCI gene amplification was highly correlated with protein overexpression (P = 0.009), suggesting that gene amplification is one important mechanism involved in PRKCI overexpression. To investigate further the role of PRKCI alteration in esophageal tumors, a tissue microarray containing samples from 180 ESCCs was used for immunohistochemistry analysis. Statistical analysis revealed that PRKCI overexpression was correlated with lymph node metastasis (P = 0.002) and higher stage (P = 0.004). Performing multivariate logistic regression analysis, a significant association between PRKCI overexpression and presence of lymph node metastasis was found, which was independent of T‐stage of the primary tumors (P = 0.004). Our results indicate that PRKCI is an attractive target in the 3q26 amplicon and that it may serve as a molecular marker for metastasis and occult advanced tumor stages in ESCC. © 2007 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/gcc.20514 |
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The aim of the present work was to identify the specific target gene from four candidates (MDS1, PRKCI, ECT2, and PIK3CA) located on 3q26 amplification in esophageal squamous cell carcinomas (ESCCs). To assess the prevalence of copy number gains of putative genes, fluorescence in situ hybridization (FISH) was applied on 108 ESCCs and 9 ESCC cell lines. Our data showed that MDS1 and PRKCI were more frequently gained. Positive correlation was found only for PRKCI between amplification and tumor size (P = 0.043), lymph node metastasis (P = 0.015) and clinical stage (P = 0.002). PRKCI gene amplification was highly correlated with protein overexpression (P = 0.009), suggesting that gene amplification is one important mechanism involved in PRKCI overexpression. To investigate further the role of PRKCI alteration in esophageal tumors, a tissue microarray containing samples from 180 ESCCs was used for immunohistochemistry analysis. Statistical analysis revealed that PRKCI overexpression was correlated with lymph node metastasis (P = 0.002) and higher stage (P = 0.004). Performing multivariate logistic regression analysis, a significant association between PRKCI overexpression and presence of lymph node metastasis was found, which was independent of T‐stage of the primary tumors (P = 0.004). Our results indicate that PRKCI is an attractive target in the 3q26 amplicon and that it may serve as a molecular marker for metastasis and occult advanced tumor stages in ESCC. © 2007 Wiley‐Liss, Inc.</description><identifier>ISSN: 1045-2257</identifier><identifier>EISSN: 1098-2264</identifier><identifier>DOI: 10.1002/gcc.20514</identifier><identifier>PMID: 17990328</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Biomarkers, Tumor - biosynthesis ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Carcinoma, Squamous Cell - enzymology ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Chromosomes, Human, Pair 3 - genetics ; Disease Progression ; Esophageal Neoplasms - enzymology ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Female ; Gene Amplification ; Gene Dosage ; Humans ; Isoenzymes - biosynthesis ; Isoenzymes - genetics ; Isoenzymes - metabolism ; Lymphatic Metastasis ; Male ; Middle Aged ; Protein Kinase C - biosynthesis ; Protein Kinase C - genetics ; Protein Kinase C - metabolism</subject><ispartof>Genes chromosomes & cancer, 2008-02, Vol.47 (2), p.127-136</ispartof><rights>Copyright © 2007 Wiley‐Liss, Inc.</rights><rights>(c) 2007 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3924-d52c5ff64f08265bdea6034c1564e57b479375903e3d9f912c4f0af4dfc37c93</citedby><cites>FETCH-LOGICAL-c3924-d52c5ff64f08265bdea6034c1564e57b479375903e3d9f912c4f0af4dfc37c93</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%2Fgcc.20514$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fgcc.20514$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17990328$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Yi-Ling</creatorcontrib><creatorcontrib>Chu, Jia-You</creatorcontrib><creatorcontrib>Luo, Man-Li</creatorcontrib><creatorcontrib>Wu, Yu-Peng</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Feng, Yan-Bin</creatorcontrib><creatorcontrib>Shi, Zhi-Zhou</creatorcontrib><creatorcontrib>Xu, Xin</creatorcontrib><creatorcontrib>Han, Ya-Ling</creatorcontrib><creatorcontrib>Cai, Yan</creatorcontrib><creatorcontrib>Dong, Jin-Tang</creatorcontrib><creatorcontrib>Zhan, Qi-Min</creatorcontrib><creatorcontrib>Wu, Min</creatorcontrib><creatorcontrib>Wang, Ming-Rong</creatorcontrib><title>Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma</title><title>Genes chromosomes & cancer</title><addtitle>Genes Chromosom. Cancer</addtitle><description>DNA amplification is one of the mechanisms to activate genes that are implicated in neoplastic transformation and gain of chromosome band 3q26 is a common event in squamous cell carcinomas. The aim of the present work was to identify the specific target gene from four candidates (MDS1, PRKCI, ECT2, and PIK3CA) located on 3q26 amplification in esophageal squamous cell carcinomas (ESCCs). To assess the prevalence of copy number gains of putative genes, fluorescence in situ hybridization (FISH) was applied on 108 ESCCs and 9 ESCC cell lines. Our data showed that MDS1 and PRKCI were more frequently gained. Positive correlation was found only for PRKCI between amplification and tumor size (P = 0.043), lymph node metastasis (P = 0.015) and clinical stage (P = 0.002). PRKCI gene amplification was highly correlated with protein overexpression (P = 0.009), suggesting that gene amplification is one important mechanism involved in PRKCI overexpression. To investigate further the role of PRKCI alteration in esophageal tumors, a tissue microarray containing samples from 180 ESCCs was used for immunohistochemistry analysis. Statistical analysis revealed that PRKCI overexpression was correlated with lymph node metastasis (P = 0.002) and higher stage (P = 0.004). Performing multivariate logistic regression analysis, a significant association between PRKCI overexpression and presence of lymph node metastasis was found, which was independent of T‐stage of the primary tumors (P = 0.004). Our results indicate that PRKCI is an attractive target in the 3q26 amplicon and that it may serve as a molecular marker for metastasis and occult advanced tumor stages in ESCC. © 2007 Wiley‐Liss, Inc.</description><subject>Biomarkers, Tumor - biosynthesis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinoma, Squamous Cell - enzymology</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Chromosomes, Human, Pair 3 - genetics</subject><subject>Disease Progression</subject><subject>Esophageal Neoplasms - enzymology</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Female</subject><subject>Gene Amplification</subject><subject>Gene Dosage</subject><subject>Humans</subject><subject>Isoenzymes - biosynthesis</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Protein Kinase C - biosynthesis</subject><subject>Protein Kinase C - genetics</subject><subject>Protein Kinase C - metabolism</subject><issn>1045-2257</issn><issn>1098-2264</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtrGzEQhUVJqHPpQ_9A0VOh4E10X-sxbGrHJLShGFL8ImStFKvdXa1Xaxz_-8ixmz6FgEDD8J3DzBwAPmN0gREil4_GXBDEMfsATjCSo4wQwY52NeOp5vkAnMb4ByEkqOQfwQDnUiJKRidgc1W3lXfe6N6HBgYH73_dFtMhrEJq2RL6BtIVEUPoI9QxBuNf2hvfL2G1rdslbEJpYW17HdNLVFLYGNqlfrS6gnG11nVYR2hsVUGjO-ObUOtzcOx0Fe2nw38GZuPvs-Imu_s5mRZXd5mhkrCs5MRw5wRzaEQEX5RWC0SZwVwwy_MFyyXNedrF0lI6iYlJpHasdIbmRtIz8HVv23ZhtbaxV7WPu0l0Y9NQKkcYE0JH74IEpXtRQRL4bQ-aLsTYWafazte62yqM1C4NldJQL2kk9svBdL2obfmfPJw_AZd7YOMru33bSU2K4p9ltlf42NunV4Xu_iqRp1Oohx8TxR7o9Ww8_63m9BkeEKKc</recordid><startdate>200802</startdate><enddate>200802</enddate><creator>Yang, Yi-Ling</creator><creator>Chu, Jia-You</creator><creator>Luo, Man-Li</creator><creator>Wu, Yu-Peng</creator><creator>Zhang, Yu</creator><creator>Feng, Yan-Bin</creator><creator>Shi, Zhi-Zhou</creator><creator>Xu, Xin</creator><creator>Han, Ya-Ling</creator><creator>Cai, Yan</creator><creator>Dong, Jin-Tang</creator><creator>Zhan, Qi-Min</creator><creator>Wu, Min</creator><creator>Wang, Ming-Rong</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</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>7T5</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200802</creationdate><title>Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma</title><author>Yang, Yi-Ling ; Chu, Jia-You ; Luo, Man-Li ; Wu, Yu-Peng ; Zhang, Yu ; Feng, Yan-Bin ; Shi, Zhi-Zhou ; Xu, Xin ; Han, Ya-Ling ; Cai, Yan ; Dong, Jin-Tang ; Zhan, Qi-Min ; Wu, Min ; Wang, Ming-Rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3924-d52c5ff64f08265bdea6034c1564e57b479375903e3d9f912c4f0af4dfc37c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Biomarkers, Tumor - biosynthesis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Carcinoma, Squamous Cell - enzymology</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Chromosomes, Human, Pair 3 - genetics</topic><topic>Disease Progression</topic><topic>Esophageal Neoplasms - enzymology</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Female</topic><topic>Gene Amplification</topic><topic>Gene Dosage</topic><topic>Humans</topic><topic>Isoenzymes - biosynthesis</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Protein Kinase C - biosynthesis</topic><topic>Protein Kinase C - genetics</topic><topic>Protein Kinase C - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Yi-Ling</creatorcontrib><creatorcontrib>Chu, Jia-You</creatorcontrib><creatorcontrib>Luo, Man-Li</creatorcontrib><creatorcontrib>Wu, Yu-Peng</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Feng, Yan-Bin</creatorcontrib><creatorcontrib>Shi, Zhi-Zhou</creatorcontrib><creatorcontrib>Xu, Xin</creatorcontrib><creatorcontrib>Han, Ya-Ling</creatorcontrib><creatorcontrib>Cai, Yan</creatorcontrib><creatorcontrib>Dong, Jin-Tang</creatorcontrib><creatorcontrib>Zhan, Qi-Min</creatorcontrib><creatorcontrib>Wu, Min</creatorcontrib><creatorcontrib>Wang, Ming-Rong</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes chromosomes & cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Yi-Ling</au><au>Chu, Jia-You</au><au>Luo, Man-Li</au><au>Wu, Yu-Peng</au><au>Zhang, Yu</au><au>Feng, Yan-Bin</au><au>Shi, Zhi-Zhou</au><au>Xu, Xin</au><au>Han, Ya-Ling</au><au>Cai, Yan</au><au>Dong, Jin-Tang</au><au>Zhan, Qi-Min</au><au>Wu, Min</au><au>Wang, Ming-Rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma</atitle><jtitle>Genes chromosomes & cancer</jtitle><addtitle>Genes Chromosom. Cancer</addtitle><date>2008-02</date><risdate>2008</risdate><volume>47</volume><issue>2</issue><spage>127</spage><epage>136</epage><pages>127-136</pages><issn>1045-2257</issn><eissn>1098-2264</eissn><abstract>DNA amplification is one of the mechanisms to activate genes that are implicated in neoplastic transformation and gain of chromosome band 3q26 is a common event in squamous cell carcinomas. The aim of the present work was to identify the specific target gene from four candidates (MDS1, PRKCI, ECT2, and PIK3CA) located on 3q26 amplification in esophageal squamous cell carcinomas (ESCCs). To assess the prevalence of copy number gains of putative genes, fluorescence in situ hybridization (FISH) was applied on 108 ESCCs and 9 ESCC cell lines. Our data showed that MDS1 and PRKCI were more frequently gained. Positive correlation was found only for PRKCI between amplification and tumor size (P = 0.043), lymph node metastasis (P = 0.015) and clinical stage (P = 0.002). PRKCI gene amplification was highly correlated with protein overexpression (P = 0.009), suggesting that gene amplification is one important mechanism involved in PRKCI overexpression. To investigate further the role of PRKCI alteration in esophageal tumors, a tissue microarray containing samples from 180 ESCCs was used for immunohistochemistry analysis. Statistical analysis revealed that PRKCI overexpression was correlated with lymph node metastasis (P = 0.002) and higher stage (P = 0.004). Performing multivariate logistic regression analysis, a significant association between PRKCI overexpression and presence of lymph node metastasis was found, which was independent of T‐stage of the primary tumors (P = 0.004). Our results indicate that PRKCI is an attractive target in the 3q26 amplicon and that it may serve as a molecular marker for metastasis and occult advanced tumor stages in ESCC. © 2007 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17990328</pmid><doi>10.1002/gcc.20514</doi><tpages>10</tpages></addata></record> |
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subjects | Biomarkers, Tumor - biosynthesis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Carcinoma, Squamous Cell - enzymology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell Line, Tumor Chromosomes, Human, Pair 3 - genetics Disease Progression Esophageal Neoplasms - enzymology Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Female Gene Amplification Gene Dosage Humans Isoenzymes - biosynthesis Isoenzymes - genetics Isoenzymes - metabolism Lymphatic Metastasis Male Middle Aged Protein Kinase C - biosynthesis Protein Kinase C - genetics Protein Kinase C - metabolism |
title | Amplification of PRKCI, located in 3q26, is associated with lymph node metastasis in esophageal squamous cell carcinoma |
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