Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer
Identifieur interne : 003F21 ( Istex/Corpus ); précédent : 003F20; suivant : 003F22Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer
Auteurs : Taek Sang Lee ; Yong Tark Jeon ; Jae Weon Kim ; Jae Kyung Won ; Noh Hyun Park ; In Ae Park ; Yong Sung Juhnn ; Soon Beom Kang ; Hyo Pyo Lee ; Yong Sang SongSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2007-01.
Abstract
Abstract: As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (P= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (P= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (P= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.
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DOI: 10.1196/annals.1397.018
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wicri:corpus="ISTEX">003F21</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer</title><author><name sortKey="Lee, Taek Sang" sort="Lee, Taek Sang" uniqKey="Lee T" first="Taek Sang" last="Lee">Taek Sang Lee</name><affiliation><mods:affiliation>Seoul Metropolitan Boramae Hospital, Seoul 156‐707, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Jeon, Yong Tark" sort="Jeon, Yong Tark" uniqKey="Jeon Y" first="Yong Tark" last="Jeon">Yong Tark Jeon</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Jae Weon" sort="Kim, Jae Weon" uniqKey="Kim J" first="Jae Weon" last="Kim">Jae Weon Kim</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Won, Jae Kyung" sort="Won, Jae Kyung" uniqKey="Won J" first="Jae Kyung" last="Won">Jae Kyung Won</name><affiliation><mods:affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Park, Noh Hyun" sort="Park, Noh Hyun" uniqKey="Park N" first="Noh Hyun" last="Park">Noh Hyun Park</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Park, In Ae" sort="Park, In Ae" uniqKey="Park I" first="In Ae" last="Park">In Ae Park</name><affiliation><mods:affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Juhnn, Yong Sung" sort="Juhnn, Yong Sung" uniqKey="Juhnn Y" first="Yong Sung" last="Juhnn">Yong Sung Juhnn</name><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kang, Soon Beom" sort="Kang, Soon Beom" uniqKey="Kang S" first="Soon Beom" last="Kang">Soon Beom Kang</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Hyo Pyo" sort="Lee, Hyo Pyo" uniqKey="Lee H" first="Hyo Pyo" last="Lee">Hyo Pyo Lee</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author><author><name sortKey="Song, Yong Sang" sort="Song, Yong Sang" uniqKey="Song Y" first="Yong Sang" last="Song">Yong Sang Song</name><affiliation><mods:affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Annals of the New York Academy of Sciences</title><title level="j" type="alt">ANNALS OF NEW YORK ACADEMY SCIENCES</title><idno type="ISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><imprint><biblScope unit="vol">1095</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="143">143</biblScope><biblScope unit="page" to="153">153</biblScope><biblScope unit="page-count">11</biblScope><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2007-01">2007-01</date></imprint><idno type="ISSN">0077-8923</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0077-8923</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Abstract: As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (P= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (P= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (P= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>vulvar</json:string><json:string>egfr</json:string><json:string>vulvar cancer</json:string><json:string>elderly patients</json:string><json:string>inflammation</json:string><json:string>receptor</json:string><json:string>inflammatory</json:string><json:string>epidermal</json:string><json:string>oncol</json:string><json:string>clinicopathologic</json:string><json:string>metastasis</json:string><json:string>cervical</json:string><json:string>node</json:string><json:string>prognostic</json:string><json:string>clin</json:string><json:string>high 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hospital</json:string></teeft></keywords><author><json:item><name>TAEK SANG LEE</name><affiliations><json:string>Seoul Metropolitan Boramae Hospital, Seoul 156‐707, Korea</json:string><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>YONG TARK JEON</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>JAE WEON KIM</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>JAE KYUNG WON</name><affiliations><json:string>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>NOH HYUN PARK</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>IN AE PARK</name><affiliations><json:string>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>YONG SUNG JUHNN</name><affiliations><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>SOON BEOM KANG</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>HYO PYO LEE</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item><json:item><name>YONG SANG SONG</name><affiliations><json:string>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string><json:string>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>vulvar cancer</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>elderly patient</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>inflammation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>COX‐2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EGFR</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>immunohistochemistry</value></json:item></subject><articleId><json:string>NYAS18</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Abstract: As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (P= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (P= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (P= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.</abstract><qualityIndicators><score>6.302</score><pdfVersion>1.3</pdfVersion><pdfPageSize>432 x 648 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1868</abstractCharCount><pdfWordCount>3302</pdfWordCount><pdfCharCount>21538</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>272</abstractWordCount></qualityIndicators><title>Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer</title><genre><json:string>article</json:string></genre><host><title>Annals of the New York Academy of 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University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0001"><persName><forename type="first">YONG TARK</forename><surname>JEON</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0002"><persName><forename type="first">JAE WEON</forename><surname>KIM</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0003"><persName><forename type="first">JAE KYUNG</forename><surname>WON</surname></persName><affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0004"><persName><forename type="first">NOH HYUN</forename><surname>PARK</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0005"><persName><forename type="first">IN AE</forename><surname>PARK</surname></persName><affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0006"><persName><forename type="first">YONG SUNG</forename><surname>JUHNN</surname></persName><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0007"><persName><forename type="first">SOON BEOM</forename><surname>KANG</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0008"><persName><forename type="first">HYO PYO</forename><surname>LEE</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><author xml:id="author-0009"><persName><forename type="first">YONG SANG</forename><surname>SONG</surname></persName><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation></author><idno type="istex">85E7A6DEA21D55C999D37D89A24293F77BB15248</idno><idno type="DOI">10.1196/annals.1397.018</idno><idno type="unit">NYAS18</idno><idno type="toTypesetVersion">file:NYAS.NYAS18.pdf</idno></analytic><monogr><title level="j" type="main">Annals of the New York Academy of Sciences</title><title level="j" type="alt">ANNALS OF NEW YORK ACADEMY SCIENCES</title><idno type="pISSN">0077-8923</idno><idno type="eISSN">1749-6632</idno><idno type="book-DOI">10.1111/(ISSN)1749-6632</idno><idno type="book-part-DOI">10.1111/nyas.2007.1095.issue-1</idno><idno type="product">NYAS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">1095</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="143">143</biblScope><biblScope unit="page" to="153">153</biblScope><biblScope unit="page-count">11</biblScope><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2007-01"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold"><hi rend="smallCaps">Abstract</hi>: </hi>
<hi rend="bold">As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (<hi rend="italic">P</hi>= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (<hi rend="italic">P</hi>= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (<hi rend="italic">P</hi>= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.</hi>
</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">vulvar cancer</term><term xml:id="k2">elderly patient</term><term xml:id="k3">inflammation</term><term xml:id="k4">COX‐2</term><term xml:id="k5">EGFR</term><term xml:id="k6">immunohistochemistry</term></keywords><classCode scheme="tocHeading1">Part I. Cancer</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/85E7A6DEA21D55C999D37D89A24293F77BB15248/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>Blackwell Publishing Inc</publisherName><publisherLoc>Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="01001"><doi origin="wiley">10.1111/nyas.2007.1095.issue-1</doi><titleGroup><title type="main">Signal Transduction Pathways, Part C: Cell Signaling in Health and Disease</title></titleGroup><numberingGroup><numbering type="journalVolume" number="1095">1095</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2007-01">January 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="18" status="forIssue"><doi origin="wiley">10.1196/annals.1397.018</doi><idGroup><id type="unit" value="NYAS18"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="tocHeading1">Part I. Cancer</title></titleGroup><eventGroup><event type="firstOnline" date="2007-03-19"></event><event type="publishedOnlineFinalForm" date="2007-03-19"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="143">143</numbering><numbering type="pageLast" number="153">153</numbering></numberingGroup><correspondenceTo>Address for correspondence: Yong Sang Song, Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul, 110‐744, Korea. Voice: +82‐2‐2072‐2822; fax: +82‐2‐762‐3599.
e‐mail: <email>yssong@snu.ac.kr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS18.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="5"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="34"></count><count type="linksCrossRef" number="41"></count></countGroup><titleGroup><title type="main">Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>TAEK SANG</givenNames><familyName>LEE</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2 #a3"><personName><givenNames>YONG TARK</givenNames><familyName>JEON</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2 #a3"><personName><givenNames>JAE WEON</givenNames><familyName>KIM</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a4"><personName><givenNames>JAE KYUNG</givenNames><familyName>WON</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2 #a3"><personName><givenNames>NOH HYUN</givenNames><familyName>PARK</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a4"><personName><givenNames>IN AE</givenNames><familyName>PARK</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>YONG SUNG</givenNames><familyName>JUHNN</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a2 #a3"><personName><givenNames>SOON BEOM</givenNames><familyName>KANG</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a2 #a3"><personName><givenNames>HYO PYO</givenNames><familyName>LEE</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a2 #a3"><personName><givenNames>YONG SANG</givenNames><familyName>SONG</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Seoul Metropolitan Boramae Hospital, Seoul 156‐707, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">vulvar cancer</keyword><keyword xml:id="k2">elderly patient</keyword><keyword xml:id="k3">inflammation</keyword><keyword xml:id="k4">COX‐2</keyword><keyword xml:id="k5">EGFR</keyword><keyword xml:id="k6">immunohistochemistry</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b><sc>Abstract</sc>: </b> <b>As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (<i>P</i>= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (<i>P</i>= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (<i>P</i>= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.</b> </p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Increased Cyclooxygenase‐2 Expression Associated with Inflammatory Cellular Infiltration in Elderly Patients with Vulvar Cancer</title></titleInfo><name type="personal"><namePart type="given">TAEK SANG</namePart><namePart type="family">LEE</namePart><affiliation>Seoul Metropolitan Boramae Hospital, Seoul 156‐707, Korea</affiliation><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YONG TARK</namePart><namePart type="family">JEON</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JAE WEON</namePart><namePart type="family">KIM</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JAE KYUNG</namePart><namePart type="family">WON</namePart><affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">NOH HYUN</namePart><namePart type="family">PARK</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">IN AE</namePart><namePart type="family">PARK</namePart><affiliation>Department of Pathology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YONG SUNG</namePart><namePart type="family">JUHNN</namePart><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SOON BEOM</namePart><namePart type="family">KANG</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HYO PYO</namePart><namePart type="family">LEE</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YONG SANG</namePart><namePart type="family">SONG</namePart><affiliation>Department of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><affiliation>Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110‐744, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2007-01</dateIssued><copyrightDate encoding="w3cdtf">2007</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">1</extent><extent unit="tables">5</extent><extent unit="references">34</extent></physicalDescription><abstract>Abstract: As the relationship between inflammation and carcinogenesis grows stronger, the role of cyclooxygenase‐2 (COX‐2) and epidermal growth factor (EGFR) has been highlighted in the pathogenesis and progression of human cancer. In view of the fact that vulvar cancer is characterized by precancerous inflammatory changes in elderly patients, the expressions of COX‐2 and EGFR are expected to show different patterns of distribution according to age and other prognostic factors. To verify whether there was a relationship between their expression and clinicopathologic parameters in vulvar cancer, we investigated the inflammatory cellular infiltration and the expression of COX‐2 and EGFR by immunohistochemical analysis. Eleven of 19 samples (57.8%) were stained positive for COX‐2, and 17 (89.4%) for EGFR. The portion of inflammatory cellular infiltration in adjacent normal tissue was also higher in the older age group, and showed a strong correlation with COX‐2 positivity (P= 0.002). Furthermore, COX‐2 expression was significantly more frequent in patients over 60 years of age compared to those under 50 years (P= 0.009). COX‐2 expression was noted to be high in moderate and well‐differentiated cases, whereas, poorly differentiated carcinoma was negative for COX‐2 expression (P= 0.023). However, EGFR expression was not differently distributed on the basis of stage, age, tumor grading, or presence of lymph node metastasis. Our article suggests that vulvar cancer in elderly patients may be associated with inflammation, and thus with increased COX‐2 expression. In light of these findings, a clinical trial designed to assess the addition of COX‐2 targeted therapy to conventional treatment in vulvar cancer would be helpful for consideration of additional treatment options and possibly avoiding the serious surgical morbidity in elderly patients.</abstract><subject lang="en"><genre>keywords</genre><topic>vulvar cancer</topic><topic>elderly patient</topic><topic>inflammation</topic><topic>COX‐2</topic><topic>EGFR</topic><topic>immunohistochemistry</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2007</date><detail type="title"><title>Signal Transduction Pathways, Part C: Cell Signaling in Health and Disease</title></detail><detail type="volume"><caption>vol.</caption><number>1095</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>143</start><end>153</end><total>11</total></extent></part></relatedItem><identifier type="istex">85E7A6DEA21D55C999D37D89A24293F77BB15248</identifier><identifier type="DOI">10.1196/annals.1397.018</identifier><identifier type="ArticleID">NYAS18</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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