The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression
Identifieur interne : 004D79 ( Istex/Corpus ); précédent : 004D78; suivant : 004D80The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression
Auteurs : Bang Wool Eom ; Min Jung Jo ; Myeong-Cherl Kook ; Keun Won Ryu ; Il Ju Choi ; Byung-Ho Nam ; Young-Woo Kim ; Jun Ho LeeSource :
- International Journal of Cancer [ 0020-7136 ] ; 2012-07-01.
Abstract
SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (p < 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (p = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.
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DOI: 10.1002/ijc.26325
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uniqKey="Eom B" first="Bang Wool" last="Eom">Bang Wool Eom</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Jo, Min Jung" sort="Jo, Min Jung" uniqKey="Jo M" first="Min Jung" last="Jo">Min Jung Jo</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kook, Myeong Herl" sort="Kook, Myeong Herl" uniqKey="Kook M" first="Myeong-Cherl" last="Kook">Myeong-Cherl Kook</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Ryu, Keun Won" sort="Ryu, Keun Won" uniqKey="Ryu K" first="Keun Won" last="Ryu">Keun Won Ryu</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Choi, Il Ju" sort="Choi, Il Ju" uniqKey="Choi I" first="Il Ju" last="Choi">Il Ju Choi</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Nam, Byung O" sort="Nam, Byung O" uniqKey="Nam B" first="Byung-Ho" last="Nam">Byung-Ho Nam</name><affiliation><mods:affiliation>Cancer Biostatistics Branch, Research Institute for National Cancer Control and Evaluation, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Young Oo" sort="Kim, Young Oo" uniqKey="Kim Y" first="Young-Woo" last="Kim">Young-Woo Kim</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jun Ho" sort="Lee, Jun Ho" uniqKey="Lee J" first="Jun Ho" last="Lee">Jun Ho Lee</name><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, 410‐769, South Korea</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">International Journal of Cancer</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF CANCER</title><idno type="ISSN">0020-7136</idno><idno type="eISSN">1097-0215</idno><imprint><biblScope unit="vol">131</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="41">41</biblScope><biblScope unit="page" to="48">48</biblScope><biblScope unit="page-count">8</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-07-01">2012-07-01</date></imprint><idno type="ISSN">0020-7136</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0020-7136</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (p < 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (p = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>gastric</json:string><json:string>gastric cancer</json:string><json:string>mrna</json:string><json:string>metastasis</json:string><json:string>lymphangiogenesis</json:string><json:string>lymphatic</json:string><json:string>angiogenesis</json:string><json:string>uicc</json:string><json:string>national cancer center</json:string><json:string>koopman</json:string><json:string>clinicopathological</json:string><json:string>node</json:string><json:string>gastric cancer tissues</json:string><json:string>gene expression</json:string><json:string>present study</json:string><json:string>gastric cancer patients</json:string><json:string>clinicopathological characteristics</json:string><json:string>elisa</json:string><json:string>positive group</json:string><json:string>peripheral 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South Korea</json:string></affiliations></json:item><json:item><name>Min Jung Jo</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Myeong‐Cherl Kook</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Keun Won Ryu</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Il Ju Choi</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Byung‐Ho Nam</name><affiliations><json:string>Cancer Biostatistics Branch, Research Institute for National Cancer Control and Evaluation, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Young‐Woo Kim</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string></affiliations></json:item><json:item><name>Jun Ho Lee</name><affiliations><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</json:string><json:string>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, 410‐769, South Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>SOX family</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SOX 18</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lymphangiogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gastric cancer</value></json:item></subject><articleId><json:string>IJC26325</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (p > 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (p = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.</abstract><qualityIndicators><score>7.307</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1645</abstractCharCount><pdfWordCount>4307</pdfWordCount><pdfCharCount>27346</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>253</abstractWordCount></qualityIndicators><title>The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression</title><genre><json:string>article</json:string></genre><host><title>International Journal of 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Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Min Jung</forename><surname>Jo</surname></persName><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Myeong‐Cherl</forename><surname>Kook</surname></persName><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Keun Won</forename><surname>Ryu</surname></persName><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Il Ju</forename><surname>Choi</surname></persName><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Byung‐Ho</forename><surname>Nam</surname></persName><affiliation>Cancer Biostatistics Branch, Research Institute for National Cancer Control and Evaluation, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Young‐Woo</forename><surname>Kim</surname></persName><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation></author><author xml:id="author-0007" role="corresp"><persName><forename type="first">Jun Ho</forename><surname>Lee</surname></persName><email>kosmas@ncc.re.kr</email><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea<address><country key="KR"></country></address></affiliation><note type="foot">Tel.: +82‐31‐920‐1629, Fax: +82‐31‐920‐0069</note><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, 410‐769, South Korea</affiliation></author><idno type="istex">A57C138EDFC24B1BC5FA23FAD4747D0835BDCBFF</idno><idno type="DOI">10.1002/ijc.26325</idno><idno type="unit">IJC26325</idno><idno type="toTypesetVersion">file:IJC.IJC26325.pdf</idno></analytic><monogr><title level="j" type="main">International Journal of Cancer</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF CANCER</title><idno type="pISSN">0020-7136</idno><idno type="eISSN">1097-0215</idno><idno type="book-DOI">10.1002/(ISSN)1097-0215</idno><idno type="book-part-DOI">10.1002/ijc.v131.1</idno><idno type="product">IJC</idno><imprint><biblScope unit="vol">131</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="41">41</biblScope><biblScope unit="page" to="48">48</biblScope><biblScope unit="page-count">8</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-07-01"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (<hi rend="italic">p</hi> < 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (<hi rend="italic">p</hi> = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">SOX family</term><term xml:id="kwd2">SOX 18</term><term xml:id="kwd3">lymphangiogenesis</term><term xml:id="kwd4">gastric cancer</term></keywords><classCode scheme="articleCategory">Cancer Cell Biology</classCode><classCode scheme="tocHeading1">Cancer Cell Biology</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/A57C138EDFC24B1BC5FA23FAD4747D0835BDCBFF/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-0215</doi><issn type="print">0020-7136</issn><issn type="electronic">1097-0215</issn><idGroup><id type="product" value="IJC"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="INTERNATIONAL JOURNAL OF CANCER">International Journal of Cancer</title><title type="short">Int. J. Cancer</title></titleGroup><selfCitationGroup><citation type="ancestor" xml:id="cit1"><journalTitle>Radiation Oncology Investigations</journalTitle><accessionId ref="info:x-wiley/issn/10657541">1065-7541</accessionId><accessionId ref="info:x-wiley/issn/15206823">1520-6823</accessionId><pubYear year="1999">1999</pubYear><vol>7</vol><issue>6</issue></citation></selfCitationGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/ijc.v131.1</doi><numberingGroup><numbering type="journalVolume" number="131">131</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2012-07-01">1 July 2012</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="50" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ijc.26325</doi><idGroup><id type="unit" value="IJC26325"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Cancer Cell Biology</title><title type="tocHeading1">Cancer Cell Biology</title></titleGroup><copyright ownership="publisher">Copyright © 2011 UICC</copyright><eventGroup><event type="manuscriptReceived" date="2011-04-06"></event><event type="manuscriptAccepted" date="2011-07-13"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.3 standalone mode:FullText" date="2012-04-20"></event><event type="publishedOnlineAccepted" date="2011-07-27"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-09-12"></event><event type="firstOnline" date="2011-09-12"></event><event type="publishedOnlineFinalForm" date="2012-04-20"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.3.7 mode:FullText" date="2015-03-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">41</numbering><numbering type="pageLast">48</numbering></numberingGroup><correspondenceTo>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, 410‐769, South Korea</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:IJC.IJC26325.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="4870"></count></countGroup><titleGroup><title type="main" xml:lang="en">The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression</title><title type="short" xml:lang="en">SOX 18 in Gastric Cancer</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Bang Wool</givenNames><familyName>Eom</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Min Jung</givenNames><familyName>Jo</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Myeong‐Cherl</givenNames><familyName>Kook</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Keun Won</givenNames><familyName>Ryu</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Il Ju</givenNames><familyName>Choi</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Byung‐Ho</givenNames><familyName>Nam</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Young‐Woo</givenNames><familyName>Kim</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes" noteRef="#fn1"><personName><givenNames>Jun Ho</givenNames><familyName>Lee</familyName></personName><contactDetails><email>kosmas@ncc.re.kr</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="KR" type="organization"><unparsedAffiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="KR" type="organization"><unparsedAffiliation>Cancer Biostatistics Branch, Research Institute for National Cancer Control and Evaluation, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">SOX family</keyword><keyword xml:id="kwd2">SOX 18</keyword><keyword xml:id="kwd3">lymphangiogenesis</keyword><keyword xml:id="kwd4">gastric cancer</keyword></keywordGroup><fundingInfo><fundingAgency>National Cancer Center, South Korea</fundingAgency><fundingNumber>0910540‐1</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (<i>p</i> < 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (<i>p</i> = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Tel.: +82‐31‐920‐1629, Fax: +82‐31‐920‐0069</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SOX 18 in Gastric Cancer</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression</title></titleInfo><name type="personal"><namePart type="given">Bang Wool</namePart><namePart type="family">Eom</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Min Jung</namePart><namePart type="family">Jo</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myeong‐Cherl</namePart><namePart type="family">Kook</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Keun Won</namePart><namePart type="family">Ryu</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Il Ju</namePart><namePart type="family">Choi</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Byung‐Ho</namePart><namePart type="family">Nam</namePart><affiliation>Cancer Biostatistics Branch, Research Institute for National Cancer Control and Evaluation, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Young‐Woo</namePart><namePart type="family">Kim</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun Ho</namePart><namePart type="family">Lee</namePart><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, South Korea</affiliation><description>Tel.: +82‐31‐920‐1629, Fax: +82‐31‐920‐0069</description><affiliation>Gastric Cancer Branch, Research Institute and Hospital, National Cancer Center, 111 Jungbalsan‐ro, Ilsandong‐gu, Goyang‐si, Gyeonggi‐do, 410‐769, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2012-07-01</dateIssued><dateCaptured encoding="w3cdtf">2011-04-06</dateCaptured><dateValid encoding="w3cdtf">2011-07-13</dateValid><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">2</extent><extent unit="references">33</extent><extent unit="words">4870</extent></physicalDescription><abstract lang="en">SOX group F genes are important regulators of angiogenesis and lymphangiogenesis. The aim of the present study was to examine the relationships between Sox group F expression and clinicopathological factors in gastric cancer. Three hundred and fifteen gastric cancer tissues and the corresponding normal gastric tissue were obtained from the tumor bank at the National Cancer Center, Korea. SOX group F mRNA levels in these tissues were evaluated by reverse transcriptase polymerase chain reaction (RT‐PCR). The serum levels of SOX 18 proteins in 219 gastric cancer patients and in 30 healthy volunteers were also measured by enzyme‐linked immunosorbent assay. Furthermore, immunohistochemistry (IHC) was performed on 679 gastric cancer tissues and the clinicopathological characteristics, as well as the survival rates of SOX 18 positive and negative gastric cancers were compared. RT‐PCR showed that SOX group F mRNA was increased in the gastric cancer tissues compared to the normal gastric tissues (p < 0.001, respectively). The serum levels of SOX 18 protein were also increased in gastric cancer patients compared to healthy volunteers. IHC showed that of the 679 gastric cancer cases, 177 (26.1%) were positive for SOX 18 expression in their tumor stroma, and the frequencies of both lymphovascular invasion and lymph node metastases were higher in the SOX 18 positive than in the negative group. Both the 5‐year survival and the recurrence‐free survival were shorter for SOX 18 positive tumors (p = 0.023 and 0.012, respectively). SOX 18 expression might be a prognostic tumor marker and a potential therapeutic target in gastric cancer.</abstract><note type="funding">National Cancer Center, South Korea - No. 0910540‐1; </note><subject lang="en"><genre>keywords</genre><topic>SOX family</topic><topic>SOX 18</topic><topic>lymphangiogenesis</topic><topic>gastric cancer</topic></subject><relatedItem type="host"><titleInfo><title>International Journal of Cancer</title></titleInfo><titleInfo type="abbreviated"><title>Int. J. Cancer</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Cancer Cell Biology</topic></subject><identifier type="ISSN">0020-7136</identifier><identifier type="eISSN">1097-0215</identifier><identifier type="DOI">10.1002/(ISSN)1097-0215</identifier><identifier type="PublisherID">IJC</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>131</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>41</start><end>48</end><total>8</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>Radiation Oncology Investigations</title></titleInfo><identifier type="ISSN">1065-7541</identifier><identifier type="ISSN">1520-6823</identifier><part><date point="end">1999</date><detail type="volume"><caption>last vol.</caption><number>7</number></detail><detail type="issue"><caption>last no.</caption><number>6</number></detail></part></relatedItem><identifier type="istex">A57C138EDFC24B1BC5FA23FAD4747D0835BDCBFF</identifier><identifier type="DOI">10.1002/ijc.26325</identifier><identifier type="ArticleID">IJC26325</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 UICC</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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