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<art>
   <ui>bcr1246</ui>
   <ji>BCJ</ji>
   <fm>
      <dochead>Poster presentation</dochead>
      <bibl>
         <title>
            <p>Expression of c-met gene in invasive ductal carcinomas</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Park</snm>
               <fnm>CH</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Lee</snm>
               <fnm>MH</fnm>
               <insr iid="I2"/>
            </au>
            <au id="A3">
               <snm>Chang</snm>
               <fnm>ES</fnm>
               <insr iid="I3"/>
            </au>
            <au id="A4">
               <snm>Song</snm>
               <fnm>BJ</fnm>
               <insr iid="I4"/>
            </au>
            <au id="A5">
               <snm>Jung</snm>
               <fnm>SS</fnm>
               <insr iid="I4"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Department of Surgery, Hallym University College of Medicine, Seoul, Korea</p>
            </ins>
            <ins id="I2">
               <p>Department of Surgery, College of Medicine, Soonchunhyang University, Cheonan, Korea</p>
            </ins>
            <ins id="I3">
               <p>Department of Surgery, College of Medicine, Chungnam National University, Daejeon, Korea</p>
            </ins>
            <ins id="I4">
               <p>Department of Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea</p>
            </ins>
         </insg>
         <source>Breast Cancer Research</source>
         <supplement>
            <title>
               <p>VI Madrid Breast Cancer Conference: Changes in the treatment of breast cancer</p>
            </title>
            <note>Meeting abstracts</note>
         </supplement>
         <conference>
            <title>
               <p>VI Madrid Breast Cancer Conference: Changes in the treatment of breast cancer</p>
            </title>
            <location>Madrid, Spain</location>
            <date-range>1&#8211;3 June 2005</date-range>
         </conference>
         <issn>1465-5411</issn>
         <pubdate>2005</pubdate>
         <volume>7</volume>
         <issue>Suppl 1</issue>
         <fpage>P12</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/bcr1246</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>27</day>
               <month>5</month>
               <year>2005</year>
            </date>
         </pub>
      </history>
   </fm>
   <bdy>
      <sec>
         <st>
            <p>Introduction</p>
         </st>
         <p>The c-Met protein, known as the hepatocyte growth factor (HGF) receptor, is a transmembrane 190 kDa heterodimer with tyrosine kinase activity, encoded by the c-met oncogene. The HGF/c-Met signalling pathway has been shown to demonstrate various cellular responses, including mitogenic, proliferative, morphogenic and angiogenic activities. Although HGF and c-Met are known to be expressed in a variety of organs and play important roles in signal transduction, studies of its expression correlated with clinico-pathological parameters in breast cancer are rare.</p>
      </sec>
      <sec>
         <st>
            <p>Method</p>
         </st>
         <p>In this study we examined c-met mRNA and c-Met protein expression by means of RT-PCR and immunohistochemical methods in 50 cases of invasive ductal carcinomas and 20 normal breast tissue samples.</p>
      </sec>
      <sec>
         <st>
            <p>Results</p>
         </st>
         <p>c-met mRNA amplification was detected in 35 cases (70%), but not in normal tissues. c-Met protein overexpression was detected in 27 cases (54%) and two cases (10%), respectively. Both mRNA amplification and protein overexpression rates were significantly higher in tumor than in normal tissue. The c-met mRNA amplification exhibited an increased tendency according to tumor invasiveness and nodal metastasis. The c-Met protein overexpression was significantly correlated with well differentiated grade and showed decreased tendency in metastatic tumor. The concordance between both mRNA amplification and protein expressions were not recognized.</p>
      </sec>
      <sec>
         <st>
            <p>Conclusion</p>
         </st>
         <p>These results suggest that HGF/c-Met signal pathway may be associated with breast cancer development. c-met mRNA amplification may play an important role in tumor progression and metastasis. c-Met protein overexpression may contribute to the morphogenesis of well differentiated tumor.</p>
      </sec>
   </bdy>
</art>
