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<art>
   <ui>bcr100</ui>
   <ji>BCJ</ji>
   <fm>
      <dochead>Meeting abstract</dochead>
      <bibl>
         <title>
            <p>Constitutional alterations of 9p23-24 in independent <it>BRCA2</it> breast cancer families</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Schwab</snm>
               <fnm>M</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Savelyeva</snm>
               <fnm>L</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A3">
               <snm>Claas</snm>
               <fnm>A</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A4">
               <snm>An</snm>
               <fnm>H</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A5">
               <snm>Brouwers</snm>
               <fnm>S</fnm>
               <insr iid="I1"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Division of Cytogenetics, German Cancer Research Center, 60120 Heidelberg, Germany</p>
            </ins>
         </insg>
         <source>Breast Cancer Res</source>
         <supplement>
            <title>
               <p>Second International Symposium on the Molecular Biology of Breast Cancer</p>
            </title>
            <note>Meeting abstracts</note>
         </supplement>
         <conference>
            <title>
               <p>Second International Symposium on the Molecular Biology of Breast Cancer</p>
            </title>
            <location>Lillehammer, Norway</location>
            <date-range>12&#8211;16 March 2000</date-range>
         </conference>
         <issn>1465-5411</issn>
         <pubdate>2000</pubdate>
         <volume>2</volume>
         <issue>Suppl 1</issue>
         <fpage>P1.13</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/bcr100</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>12</day>
               <month>3</month>
               <year>2000</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2000</year>
         <collab>Current Science Ltd</collab>
      </cpyrt>
   </fm>
   <meta>
      <classifications>
         <classification type="BMC" subtype="old_arx_id">bcr-2-S1-P1-13</classification>
      </classifications>
   </meta>
   <bdy>
      <sec>
         <st>
            <p>Full text</p>
         </st>
         <p>Germ line mutations of <it>BRCA2</it> are predicted to account for the majority of families with both male and female breast cancer. However, there is circumstantial evidence that the cancer risk conferred by <it>BRCA2</it> mutation may be modified by other genetic or environmental factors. By employing a combination of classical G-banding and fluorescence <it>in situ</it> hybridization analyses we have identified chromosomal alterations on 9p23-24 in peripheral lymphocytes of independent <it>BRCA2</it> breast cancer patients. Tandem duplication and amplification with inversion are constitutional rearrangements in four male breast cancer patients from two high-risk families. Interstitial deletion of the same region was found in four male and one female patients from an independent family. The biological significance of the coexistence of <it>BRCA2</it> mutation and 9p23-24 abnormalities in breast cancer families may be complex. Possible explanations include (1) the <it>BRCA2</it> mutation is related to the 9p-rearrangement, or (2) the 9p rearrangement is elicited by another as yet unknown factor, and chromosomal changes on 9p could be related to modifying cancer risk.</p>
      </sec>
   </bdy>
</art>
