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<art>
   <ui>bcr1099</ui>
   <ji>BCJ</ji>
   <fm>
      <dochead>Poster Presentation</dochead>
      <bibl>
         <title>
            <p>Who gets cancer?</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Nex&#248;</snm>
               <fnm>BA</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Vogel</snm>
               <fnm>U</fnm>
               <insr iid="I2"/>
            </au>
            <au id="A3">
               <snm>Overvad</snm>
               <fnm>K</fnm>
               <insr iid="I3"/>
            </au>
            <au id="A4">
               <snm>Raaschou-Nielsen</snm>
               <fnm>O</fnm>
               <insr iid="I4"/>
            </au>
            <au id="A5">
               <snm>Tj&#248;nneland</snm>
               <fnm>A</fnm>
               <insr iid="I4"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Institute of Human Genetics, University of Aarhus, Denmark</p>
            </ins>
            <ins id="I2">
               <p>National Institute of Occupational Health, Copenhagen, Denmark</p>
            </ins>
            <ins id="I3">
               <p>Department of Clinical Epidemiology, Aalborg Hospital and Aarhus University Hospital, and Department of Epidemiology and Social Medicine, University of Aarhus, Denmark</p>
            </ins>
            <ins id="I4">
               <p>Institute of Cancer Epidemiology, The Danish Cancer Society, Copenhagen, Denmark</p>
            </ins>
         </insg>
         <source>Breast Cancer Research</source>
         <supplement>
            <title>
               <p>The Third International Symposium on the Molecular Biology of Breast Cancer</p>
            </title>
            <sponsor>
               <note>Affymetrix, Agilent Technologies, Applied Biosystems, AstraZeneca, Novartis Oncology, Pfizer, Roche Diagnostics (Main Sponsors).</note>
            </sponsor>
            <note>Meeting abstracts</note>
         </supplement>
         <conference>
            <title>
               <p>The Third International Symposium on the Molecular Biology of Breast Cancer</p>
            </title>
            <location>Molde, Norway</location>
            <date-range>22&#8211;26 June 2005</date-range>
         </conference>
         <issn>1465-5411</issn>
         <pubdate>2005</pubdate>
         <volume>7</volume>
         <issue>Suppl 2</issue>
         <fpage>P1.12</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/bcr1099</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>17</day>
               <month>6</month>
               <year>2005</year>
            </date>
         </pub>
      </history>
   </fm>
   <bdy>
      <sec>
         <st>
            <p/>
         </st>
         <p>We have looked for genetic differences influencing cancer risk in the general human population. One human chromosomal region that recent data indicate as important for cancer risk is 19q13.2-3, more specifically a 69 kb region including the genes <it>XPD</it>, <it>RAI</it>, <it>ASE1 </it>and <it>ERCC1</it>. We and others have produced evidence of association between this region and occurrence of a variety of cancers, including basal cell carcinoma, melanoma, lung cancer, glioma, breast cancer, bladder cancer, and possibly head and neck cancer (see for instance <abbrgrp><abbr bid="B1">1</abbr></abbrgrp>). A recent search along the region for markers with maximal association to basal cell carcinoma has led to a focus on the gene <it>RAI </it><abbrgrp><abbr bid="B2">2</abbr></abbrgrp>. Moreover, the effect appears to be strongest among fairly young persons (&lt;56 years of age).</p>
         <p>These studies mainly involved analysis of single nucleotide polymorphisms in unrelated cases and controls. However, other studies have mapped a glioma tumor suppressor function to an almost overlapping region using deletions in tumor DNA <abbrgrp><abbr bid="B3">3</abbr></abbrgrp>. Finally, a recent genome-wide scan for chromosomal regions associated with aggressive prostate cancer located the strongest effector in a 6 Mb region, which includes the four genes mentioned <abbrgrp><abbr bid="B4">4</abbr></abbrgrp>.</p>
         <p>It appears that this region of chromosome 19, most probably the gene <it>RAI</it>, often contains a genetic variant, which increases the risk of several cancers among fairly young humans. <it>RAI </it>produces an inhibitor of NF-&#954; B, and may thus be involved in apoptosis, which makes it very easy to rationalize its importance for cancer. In addition, studies of lung cancer have produced evidence for an independent effector within the 69 kb region of interest, possibly related to DNA repair.</p>
      </sec>
   </bdy>
   <bm>
      <refgrp>
         <bibl id="B1">
            <title>
               <p>A specific haplotype of single nucleotide polymorphisms on chromosome 19q13.2-3 encompassing the genes RAI is indicative of postmenopausal breast cancer before age 55</p>
            </title>
            <aug>
               <au>
                  <snm>Nex&#248;</snm>
                  <fnm>BA</fnm>
               </au>
               <au>
                  <snm>Vogel</snm>
                  <fnm>U</fnm>
               </au>
               <au>
                  <snm>Olsen</snm>
                  <fnm>A</fnm>
               </au>
               <au>
                  <snm>Ketelsen</snm>
                  <fnm>T</fnm>
               </au>
               <au>
                  <snm>Bukowy</snm>
                  <fnm>Z</fnm>
               </au>
               <au>
                  <snm>Thomsen</snm>
                  <fnm>BL</fnm>
               </au>
               <au>
                  <snm>Wallin</snm>
                  <fnm>H</fnm>
               </au>
               <au>
                  <snm>Overvad</snm>
                  <fnm>K</fnm>
               </au>
               <au>
                  <snm>Tj&#248;nneland</snm>
                  <fnm>A</fnm>
               </au>
            </aug>
            <source>Carcinogenesis</source>
            <pubdate>2003</pubdate>
            <volume>24</volume>
            <fpage>899</fpage>
            <lpage>904</lpage>
            <xrefbib>
               <pubidlist>
                  <pubid idtype="doi">10.1093/carcin/bgg043</pubid>
                  <pubid idtype="pmpid" link="fulltext">12771034</pubid>
               </pubidlist>
            </xrefbib>
         </bibl>
         <bibl id="B2">
            <title>
               <p>Association of chromosome 19q13.2-3 with basal cell carcinoma: tentative delineation of an involved region using data for single nucleotide polymorphisms in two cohorts</p>
            </title>
            <aug>
               <au>
                  <snm>Rockenbauer</snm>
                  <fnm>E</fnm>
               </au>
               <au>
                  <snm>Bendixen</snm>
                  <fnm>MH</fnm>
               </au>
               <au>
                  <snm>Bukowy</snm>
                  <fnm>Z</fnm>
               </au>
               <au>
                  <snm>Yin</snm>
                  <fnm>J</fnm>
               </au>
               <au>
                  <snm>Jacobsen</snm>
                  <fnm>NR</fnm>
               </au>
               <au>
                  <snm>Hedayati</snm>
                  <fnm>MA</fnm>
               </au>
               <au>
                  <snm>Vogel</snm>
                  <fnm>U</fnm>
               </au>
               <au>
                  <snm>Grossman</snm>
                  <fnm>L</fnm>
               </au>
               <au>
                  <snm>Bolund</snm>
                  <fnm>L</fnm>
               </au>
               <au>
                  <snm>Nex&#248;</snm>
                  <fnm>BA</fnm>
               </au>
            </aug>
            <source>Carcinogenesis</source>
            <pubdate>2002</pubdate>
            <volume>23</volume>
            <fpage>1149</fpage>
            <lpage>1153</lpage>
            <xrefbib>
               <pubidlist>
                  <pubid idtype="doi">10.1093/carcin/23.7.1149</pubid>
                  <pubid idtype="pmpid" link="fulltext">12117772</pubid>
               </pubidlist>
            </xrefbib>
         </bibl>
         <bibl id="B3">
            <title>
               <p>Transcript map of the 23.7 Mb D19S112-D19S246 candidate tumor suppressor region on the long arm of chromosome 19</p>
            </title>
            <aug>
               <au>
                  <snm>Hartmann</snm>
                  <fnm>C</fnm>
               </au>
               <au>
                  <snm>Johnk</snm>
                  <fnm>L</fnm>
               </au>
               <au>
                  <snm>Kitange</snm>
                  <fnm>G</fnm>
               </au>
               <au>
                  <snm>Wu</snm>
                  <fnm>Y</fnm>
               </au>
               <au>
                  <snm>Ashworth</snm>
                  <fnm>LK</fnm>
               </au>
               <au>
                  <snm>Jenkins</snm>
                  <fnm>RB</fnm>
               </au>
               <au>
                  <snm>Louis</snm>
                  <fnm>DN</fnm>
               </au>
            </aug>
            <source>Cancer Res</source>
            <pubdate>2002</pubdate>
            <volume>62</volume>
            <fpage>4100</fpage>
            <lpage>4108</lpage>
            <xrefbib>
               <pubid idtype="pmpid" link="fulltext">12124348</pubid>
            </xrefbib>
         </bibl>
         <bibl id="B4">
            <title>
               <p>Confirmation of linkage of prostate cancer aggressiveness with chromosome 19q</p>
            </title>
            <aug>
               <au>
                  <snm>Slager</snm>
                  <fnm>SL</fnm>
               </au>
               <au>
                  <snm>Schaid</snm>
                  <fnm>DJ</fnm>
               </au>
               <au>
                  <snm>Cunningham</snm>
                  <fnm>JM</fnm>
               </au>
               <au>
                  <snm>McDonnell</snm>
                  <fnm>SK</fnm>
               </au>
               <au>
                  <snm>Marks</snm>
                  <fnm>AF</fnm>
               </au>
               <au>
                  <snm>Peterson</snm>
                  <fnm>BJ</fnm>
               </au>
               <au>
                  <snm>Hebbring</snm>
                  <fnm>SJ</fnm>
               </au>
               <au>
                  <snm>Anderson</snm>
                  <fnm>S</fnm>
               </au>
               <au>
                  <snm>French</snm>
                  <fnm>AJ</fnm>
               </au>
               <au>
                  <snm>Thibodeau</snm>
                  <fnm>SN</fnm>
               </au>
            </aug>
            <source>Am J Hum Genet</source>
            <pubdate>2003</pubdate>
            <volume>72</volume>
            <fpage>759</fpage>
            <lpage>762</lpage>
            <xrefbib>
               <pubidlist>
                  <pubid idtype="doi">10.1086/368230</pubid>
                  <pubid idtype="pmpid" link="fulltext">12563560</pubid>
               </pubidlist>
            </xrefbib>
         </bibl>
      </refgrp>
   </bm>
</art>
