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   <ui>gb-spotlight-20010816-01</ui>
   <ji>GBJ</ji>
   <fm>
      <dochead>Research news</dochead>
      <bibl>
         <title>
            <p>A pathway to therapeutic destruction</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Toma</snm>
               <fnm>Tudor</fnm>
               <email>t.toma@ic.ac.uk</email>
            </au>
         </aug>
         <source>Genome Biology</source>
         <issn>1465-6906</issn>
         <pubdate>2001</pubdate>
         <volume>2</volume>
         <fpage>spotlight-20010816-01</fpage>
         <xrefbib>
            <pubid idtype="doi">10.1186/gb-spotlight-20010816-01</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>16</day>
               <month>08</month>
               <year>2001</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2001</year>
         <collab>BioMed Central Ltd</collab>
      </cpyrt>
      <shortabs>
         <p>Pancreatic cancer cells have an intact proapoptotic pathway activated by interferon gamma via caspase-1 dependent mechanisms.</p>
      </shortabs>
   </fm>
   <meta>
      <classifications>
         <classification type="STATUS">Archive</classification>
      </classifications>
   </meta>
   <bdy>
      <sec>
         <st>
            <p/>
         </st>
         <p>Pancreatic cancers contain defective apoptotic pathways, making the tumor cells resistant to current chemotherapy regimes. But, in the August issue of <abbr bid="B1"><it>Gut</it></abbr>, Detjen and colleagues from the <abbr bid="B2">Humboldt University</abbr>, Berlin show that there is still an intact proapoptotic pathway in pancreatic cancer cells activated by interferon ? (IFN-?) and/or procaspase-1 which may have therapeutic potential.</p>
         <p>Detjen <it>et al.</it> found that treatment with IFN-? of four human pancreatic cancer cell lines profoundly inhibited growth of cancer cells. Cell cycle analyses revealed subdiploid cells suggesting apoptosis, which was confirmed by demonstration of DNA fragmentation. Apoptosis was preceded by upregulation of procaspase-1 and the caspase inhibitor z-vad-fmk completely prevented IFN-? apoptotic effects (<it>Gut</it> 2001, <b>49</b>:251-262).</p>
         <p>Understanding of the prevalent defects in cell cycle control as well as detection of intact proapoptotic pathways in cancer cells may help to define new anti-tumoral strategies.</p>
      </sec>
   </bdy>
   <bm>
      <refgrp>
         <bibl id="B1">
            <url>http://gut.bmjjournals.com/cgi/content/abstract/49/2/251 </url>
            <note>Detjen KM, Farwig K, Welzel M, Wiedenmann B, Rosewicz S: <b>Interferon ? inhibits growth of human pancreatic carcinoma cells via caspase-1 dependent induction of apoptosis.</b><it> Gut</it> 2001, <b> 49:</b>251-262. </note>
         </bibl>
         <bibl id="B2">
            <url>http://www.hu-berlin.de/indexe.html </url>
            <note>Humboldt University</note>
         </bibl>
      </refgrp>
   </bm>
</art>
