Immunity against Cyclin B1 Tumor Antigen Delays Development of Spontaneous Cyclin B1‐Positive Tumors in p53−/− Mice
Identifieur interne : 000088 ( Istex/Corpus ); précédent : 000087; suivant : 000089Immunity against Cyclin B1 Tumor Antigen Delays Development of Spontaneous Cyclin B1‐Positive Tumors in p53−/− Mice
Auteurs : Laura A. Vella ; Min Yu ; Amy B. Phillips ; Olivera J. FinnSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2009-09.
English descriptors
- KwdEn :
- Abnormal expression, Amersham biosciences, Breast cancer, Cancer patients, Cancer vaccines, Carcinoma, Cell carcinoma, Cell cycle, Cell lung cancer, Clinical implication, Cyclin, Cyclin tumors, Elisa plates, Empty vector, Gastric cancer, Healthy individuals, High expression, Immune, Immune response, Immune responses, Immunohistochemical staining, Iomai corporation, Mice overexpress cyclin, Mouse, Mouse cyclin, Normal cells, Overall survival, Overexpress cyclin, Overexpressed cyclin, Overexpression, Primary tumor, Prognostic implications, Spontaneous cyclin tumors, Squamous cell carcinoma, Tumor antigen, Tumor cells, Tumor cells metastasizing, Tumor growth, Vaccination, Vaccine, Vaccine delays, Vella, York academy.
- Teeft :
- Abnormal expression, Amersham biosciences, Breast cancer, Cancer patients, Cancer vaccines, Carcinoma, Cell carcinoma, Cell cycle, Cell lung cancer, Clinical implication, Cyclin, Cyclin tumors, Elisa plates, Empty vector, Gastric cancer, Healthy individuals, High expression, Immune, Immune response, Immune responses, Immunohistochemical staining, Iomai corporation, Mice overexpress cyclin, Mouse, Mouse cyclin, Normal cells, Overall survival, Overexpress cyclin, Overexpressed cyclin, Overexpression, Primary tumor, Prognostic implications, Spontaneous cyclin tumors, Squamous cell carcinoma, Tumor antigen, Tumor cells, Tumor cells metastasizing, Tumor growth, Vaccination, Vaccine, Vaccine delays, Vella, York academy.
Abstract
We previously identified cyclin B1‐specific T cells and antibodies in cancer patients with cyclin B1‐positive (+) tumors and also in some healthy individuals. We also demonstrated that these responses may be important in cancer immunosurveillance by showing that vaccination against cyclin B1 prevents growth of transplantable cyclin B1+ tumors in mice. Constitutive overexpression of cyclin B1 was determined to correlate with the lack of p53 function. This allowed us to use p53−/− mice as a model that better approximates human disease. These p53−/− mice spontaneously develop cyclin B1+ tumors. At 5–6 weeks of age, when the mice were still healthy with no evidence of tumor, they received the cyclin B1 vaccine and were then observed for tumor growth. We demonstrate that cyclin B1 vaccination delays spontaneous cyclin B1+ tumor growth and increases median survival of tumor‐bearing p53−/− mice.
Url:
DOI: 10.1111/j.1749-6632.2009.04941.x
Links to Exploration step
ISTEX:041B0040891D70751988E29D51769B13AF7CE5A5Le document en format XML
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We also demonstrated that these responses may be important in cancer immunosurveillance by showing that vaccination against cyclin B1 prevents growth of transplantable cyclin B1+ tumors in mice. Constitutive overexpression of cyclin B1 was determined to correlate with the lack of p53 function. This allowed us to use p53−/− mice as a model that better approximates human disease. These p53−/− mice spontaneously develop cyclin B1+ tumors. At 5–6 weeks of age, when the mice were still healthy with no evidence of tumor, they received the cyclin B1 vaccine and were then observed for tumor growth. 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We also demonstrated that these responses may be important in cancer immunosurveillance by showing that vaccination against cyclin B1 prevents growth of transplantable cyclin B1<hi rend="superscript">+</hi> tumors in mice. Constitutive overexpression of cyclin B1 was determined to correlate with the lack of p53 function. This allowed us to use p53<hi rend="superscript">−/−</hi> mice as a model that better approximates human disease. These p53<hi rend="superscript">−/−</hi> mice spontaneously develop cyclin B1<hi rend="superscript">+</hi> tumors. At 5–6 weeks of age, when the mice were still healthy with no evidence of tumor, they received the cyclin B1 vaccine and were then observed for tumor growth. We demonstrate that cyclin B1 vaccination delays spontaneous cyclin B1<hi rend="superscript">+</hi> tumor growth and increases median survival of tumor‐bearing p53<hi rend="superscript">−/−</hi> mice.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">cancer vaccines</term><term xml:id="k2">immunosurveillance</term><term xml:id="k3">mouse model</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></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/041B0040891D70751988E29D51769B13AF7CE5A5/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="11741"><doi origin="wiley">10.1111/nyas.2009.1174.issue-1</doi><titleGroup><title type="main">Cancer Vaccines Sixth International Symposium</title></titleGroup><numberingGroup><numbering type="journalVolume" number="11741">1174</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2009-09">September 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="9" status="forIssue"><doi origin="wiley">10.1111/j.1749-6632.2009.04941.x</doi><idGroup><id type="unit" value="NYAS4941"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2009 New York Academy of Sciences</copyright><eventGroup><event type="firstOnline" date="2009-09-14"></event><event type="publishedOnlineFinalForm" date="2009-09-14"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.4 mode:FullText" date="2011-01-31"></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="68">68</numbering><numbering type="pageLast" number="73">73</numbering></numberingGroup><correspondenceTo>Address for corresondence: Olivera J. Finn, E1040 Biological Sciences Tower, 200 Lothrop Street, Pittsburgh, PA 15261. Voice 412‐648‐9816; fax: 412‐648‐7042. <email>ojfinn@pitt.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS4941.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="26"></count><count type="linksCrossRef" number="18"></count></countGroup><titleGroup><title type="main">Immunity against Cyclin B1 Tumor Antigen Delays Development of Spontaneous Cyclin B1‐Positive Tumors in p53<sup>−/−</sup> Mice</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Laura A.</givenNames><familyName>Vella</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Min</givenNames><familyName>Yu</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Amy B.</givenNames><familyName>Phillips</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Olivera J.</givenNames><familyName>Finn</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">cancer vaccines</keyword><keyword xml:id="k2">immunosurveillance</keyword><keyword xml:id="k3">mouse model</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>We previously identified cyclin B1‐specific T cells and antibodies in cancer patients with cyclin B1‐positive (+) tumors and also in some healthy individuals. We also demonstrated that these responses may be important in cancer immunosurveillance by showing that vaccination against cyclin B1 prevents growth of transplantable cyclin B1<sup>+</sup> tumors in mice. Constitutive overexpression of cyclin B1 was determined to correlate with the lack of p53 function. This allowed us to use p53<sup>−/−</sup> mice as a model that better approximates human disease. These p53<sup>−/−</sup> mice spontaneously develop cyclin B1<sup>+</sup> tumors. At 5–6 weeks of age, when the mice were still healthy with no evidence of tumor, they received the cyclin B1 vaccine and were then observed for tumor growth. We demonstrate that cyclin B1 vaccination delays spontaneous cyclin B1<sup>+</sup> tumor growth and increases median survival of tumor‐bearing p53<sup>−/−</sup> mice.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Immunity against Cyclin B1 Tumor Antigen Delays Development of Spontaneous Cyclin B1‐Positive Tumors in p53−/− Mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Immunity against Cyclin B1 Tumor Antigen Delays Development of Spontaneous Cyclin B1‐Positive Tumors in p53−/− Mice</title></titleInfo><name type="personal"><namePart type="given">Laura A.</namePart><namePart type="family">Vella</namePart><affiliation>Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Min</namePart><namePart type="family">Yu</namePart><affiliation>Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Amy B.</namePart><namePart type="family">Phillips</namePart><affiliation>Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olivera J.</namePart><namePart type="family">Finn</namePart><affiliation>Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2009-09</dateIssued><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">2</extent><extent unit="tables">0</extent><extent unit="formulas">0</extent><extent unit="references">26</extent><extent unit="linksCrossRef">18</extent></physicalDescription><abstract lang="en">We previously identified cyclin B1‐specific T cells and antibodies in cancer patients with cyclin B1‐positive (+) tumors and also in some healthy individuals. We also demonstrated that these responses may be important in cancer immunosurveillance by showing that vaccination against cyclin B1 prevents growth of transplantable cyclin B1+ tumors in mice. Constitutive overexpression of cyclin B1 was determined to correlate with the lack of p53 function. This allowed us to use p53−/− mice as a model that better approximates human disease. These p53−/− mice spontaneously develop cyclin B1+ tumors. At 5–6 weeks of age, when the mice were still healthy with no evidence of tumor, they received the cyclin B1 vaccine and were then observed for tumor growth. We demonstrate that cyclin B1 vaccination delays spontaneous cyclin B1+ tumor growth and increases median survival of tumor‐bearing p53−/− mice.</abstract><subject lang="en"><genre>keywords</genre><topic>cancer vaccines</topic><topic>immunosurveillance</topic><topic>mouse model</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">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>2009</date><detail type="title"><title>Cancer Vaccines Sixth International Symposium</title></detail><detail type="volume"><caption>vol.</caption><number>1174</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>68</start><end>73</end><total>6</total></extent></part></relatedItem><identifier type="istex">041B0040891D70751988E29D51769B13AF7CE5A5</identifier><identifier type="ark">ark:/67375/WNG-8Z0TZXVL-T</identifier><identifier type="DOI">10.1111/j.1749-6632.2009.04941.x</identifier><identifier type="ArticleID">NYAS4941</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 New York Academy of Sciences</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/041B0040891D70751988E29D51769B13AF7CE5A5/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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