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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>KDR</italic> Activating Mutations in Human Angiosarcomas are Sensitive to Specific Kinase Inhibitors</title><author><name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R" last="Antonescu">Cristina R. Antonescu</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Yoshida, Akihiko" sort="Yoshida, Akihiko" uniqKey="Yoshida A" first="Akihiko" last="Yoshida">Akihiko Yoshida</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Guo, Tianhuo" sort="Guo, Tianhuo" uniqKey="Guo T" first="Tianhuo" last="Guo">Tianhuo Guo</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Chang, Ning En" sort="Chang, Ning En" uniqKey="Chang N" first="Ning-En" last="Chang">Ning-En Chang</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Agaram, Narasimhan P" sort="Agaram, Narasimhan P" uniqKey="Agaram N" first="Narasimhan P" last="Agaram">Narasimhan P. Agaram</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Qin, Li Xuan" sort="Qin, Li Xuan" uniqKey="Qin L" first="Li-Xuan" last="Qin">Li-Xuan Qin</name><affiliation><nlm:aff id="A2"> Departments of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Brennan, Murray F" sort="Brennan, Murray F" uniqKey="Brennan M" first="Murray F." last="Brennan">Murray F. Brennan</name><affiliation><nlm:aff id="A3"> Departments of Surgery, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Singer, Samuel" sort="Singer, Samuel" uniqKey="Singer S" first="Samuel" last="Singer">Samuel Singer</name><affiliation><nlm:aff id="A3"> Departments of Surgery, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Maki, Robert G" sort="Maki, Robert G" uniqKey="Maki R" first="Robert G" last="Maki">Robert G. Maki</name><affiliation><nlm:aff id="A4"> Departments of Medicine, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19723655</idno><idno type="pmc">2763376</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763376</idno><idno type="RBID">PMC:2763376</idno><idno type="doi">10.1158/0008-5472.CAN-09-2068</idno><date when="2009">2009</date><idno type="wicri:Area/Pmc/Corpus">002837</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002837</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>KDR</italic> Activating Mutations in Human Angiosarcomas are Sensitive to Specific Kinase Inhibitors</title><author><name sortKey="Antonescu, Cristina R" sort="Antonescu, Cristina R" uniqKey="Antonescu C" first="Cristina R" last="Antonescu">Cristina R. Antonescu</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Yoshida, Akihiko" sort="Yoshida, Akihiko" uniqKey="Yoshida A" first="Akihiko" last="Yoshida">Akihiko Yoshida</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Guo, Tianhuo" sort="Guo, Tianhuo" uniqKey="Guo T" first="Tianhuo" last="Guo">Tianhuo Guo</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Chang, Ning En" sort="Chang, Ning En" uniqKey="Chang N" first="Ning-En" last="Chang">Ning-En Chang</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Agaram, Narasimhan P" sort="Agaram, Narasimhan P" uniqKey="Agaram N" first="Narasimhan P" last="Agaram">Narasimhan P. Agaram</name><affiliation><nlm:aff id="A1"> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Qin, Li Xuan" sort="Qin, Li Xuan" uniqKey="Qin L" first="Li-Xuan" last="Qin">Li-Xuan Qin</name><affiliation><nlm:aff id="A2"> Departments of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Brennan, Murray F" sort="Brennan, Murray F" uniqKey="Brennan M" first="Murray F." last="Brennan">Murray F. Brennan</name><affiliation><nlm:aff id="A3"> Departments of Surgery, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Singer, Samuel" sort="Singer, Samuel" uniqKey="Singer S" first="Samuel" last="Singer">Samuel Singer</name><affiliation><nlm:aff id="A3"> Departments of Surgery, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author><author><name sortKey="Maki, Robert G" sort="Maki, Robert G" uniqKey="Maki R" first="Robert G" last="Maki">Robert G. Maki</name><affiliation><nlm:aff id="A4"> Departments of Medicine, Memorial Sloan-Kettering Cancer, New York, NY</nlm:aff></affiliation></author></analytic><series><title level="j">Cancer research</title><idno type="ISSN">0008-5472</idno><idno type="eISSN">1538-7445</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Angiosarcomas (AS) represent a heterogeneous group of malignant vascular tumors occurring not only in different anatomic locations, but also in distinct clinical settings, such as radiation or associated chronic lymphedema. While representing only 1–2% of soft tissue sarcomas, vascular sarcomas provide unique insight into the general process of tumor angiogenesis. However, no molecular candidates have been identified to guide a specific therapeutic intervention. By expression profiling AS show distinct up-regulation of vascular-specific receptor tyrosine kinases, including <italic>TIE1</italic>, <italic>KDR</italic>, <italic>SNRK</italic>, <italic>TEK</italic>, and <italic>FLT1</italic>. Full-sequencing of these five candidate genes identified 10% of patients harboring <italic>KDR</italic> mutations. A <italic>KDR</italic>-positive genotype was associated with strong KDR protein expression and was restricted to the breast anatomic site, with or without prior exposure to radiation. Transient transfection of <italic>KDR</italic> mutants into COS-7 cells demonstrated ligand-independent activation of the kinase, which was inhibited by specific KDR inhibitors. These data provide a basis for the activity of VEGFR-directed therapy in the treatment of primary and radiation-induced angiosarcoma.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2984705R</journal-id><journal-id journal-id-type="pubmed-jr-id">2786</journal-id><journal-id journal-id-type="nlm-ta">Cancer Res</journal-id><journal-title>Cancer research</journal-title><issn pub-type="ppub">0008-5472</issn><issn pub-type="epub">1538-7445</issn></journal-meta><article-meta><article-id pub-id-type="pmid">19723655</article-id><article-id pub-id-type="pmc">2763376</article-id><article-id pub-id-type="doi">10.1158/0008-5472.CAN-09-2068</article-id><article-id pub-id-type="manuscript">NIHMS135278</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title><italic>KDR</italic> Activating Mutations in Human Angiosarcomas are Sensitive to Specific Kinase Inhibitors</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Antonescu</surname><given-names>Cristina R</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Yoshida</surname><given-names>Akihiko</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Guo</surname><given-names>Tianhuo</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Chang</surname><given-names>Ning-En</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Lei</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Agaram</surname><given-names>Narasimhan P</given-names></name><xref rid="A1" ref-type="aff">1</xref></contrib><contrib contrib-type="author"><name><surname>Qin</surname><given-names>Li-Xuan</given-names></name><xref rid="A2" ref-type="aff">2</xref></contrib><contrib contrib-type="author"><name><surname>Brennan</surname><given-names>Murray F.</given-names></name><xref rid="A3" ref-type="aff">3</xref></contrib><contrib contrib-type="author"><name><surname>Singer</surname><given-names>Samuel</given-names></name><xref rid="A3" ref-type="aff">3</xref></contrib><contrib contrib-type="author"><name><surname>Maki</surname><given-names>Robert G</given-names></name><xref rid="A4" ref-type="aff">4</xref></contrib></contrib-group><aff id="A1"><label>1</label> Departments of Pathology, Memorial Sloan-Kettering Cancer, New York, NY</aff><aff id="A2"><label>2</label> Departments of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer, New York, NY</aff><aff id="A3"><label>3</label> Departments of Surgery, Memorial Sloan-Kettering Cancer, New York, NY</aff><aff id="A4"><label>4</label> Departments of Medicine, Memorial Sloan-Kettering Cancer, New York, NY</aff><author-notes><corresp id="FN1">Correspondance: Cristina R. Antonescu, MD, Department of Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, Tel: 212-639-5721, Fax: 212-717-3203, <email>antonesc@mskcc.org</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>4</day><month>8</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>1</day><month>9</month><year>2009</year></pub-date><pub-date pub-type="ppub"><day>15</day><month>9</month><year>2009</year></pub-date><pub-date pub-type="pmc-release"><day>15</day><month>9</month><year>2010</year></pub-date><volume>69</volume><issue>18</issue><fpage>7175</fpage><lpage>7179</lpage><abstract><p id="P1">Angiosarcomas (AS) represent a heterogeneous group of malignant vascular tumors occurring not only in different anatomic locations, but also in distinct clinical settings, such as radiation or associated chronic lymphedema. While representing only 1–2% of soft tissue sarcomas, vascular sarcomas provide unique insight into the general process of tumor angiogenesis. However, no molecular candidates have been identified to guide a specific therapeutic intervention. By expression profiling AS show distinct up-regulation of vascular-specific receptor tyrosine kinases, including <italic>TIE1</italic>, <italic>KDR</italic>, <italic>SNRK</italic>, <italic>TEK</italic>, and <italic>FLT1</italic>. Full-sequencing of these five candidate genes identified 10% of patients harboring <italic>KDR</italic> mutations. A <italic>KDR</italic>-positive genotype was associated with strong KDR protein expression and was restricted to the breast anatomic site, with or without prior exposure to radiation. Transient transfection of <italic>KDR</italic> mutants into COS-7 cells demonstrated ligand-independent activation of the kinase, which was inhibited by specific KDR inhibitors. These data provide a basis for the activity of VEGFR-directed therapy in the treatment of primary and radiation-induced angiosarcoma.</p></abstract><kwd-group><kwd>angiosarcoma</kwd><kwd>KDR</kwd><kwd>kinase inhibitors</kwd><kwd>sorafenib</kwd><kwd>sunitinib</kwd></kwd-group><contract-num rid="CA1">P01 CA047179-15A29002</contract-num><contract-sponsor id="CA1">National Cancer Institute : NCI</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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