<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1409-0015</journal-id>
<journal-title><![CDATA[Medicina Legal de Costa Rica]]></journal-title>
<abbrev-journal-title><![CDATA[Med. leg. Costa Rica]]></abbrev-journal-title>
<issn>1409-0015</issn>
<publisher>
<publisher-name><![CDATA[Asociación Costarricense de Medicina Forense]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1409-00152018000100003</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Cáncer de páncreas: alteraciones genéticas, cambios morfológicos y sus implicaciones terapéuticas]]></article-title>
<article-title xml:lang="en"><![CDATA[Pancreas cancer: genetic alterations, morphological changes and its therapeutic implications]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Madrigal Ureña]]></surname>
<given-names><![CDATA[Angélica]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[García Chaves]]></surname>
<given-names><![CDATA[Daniela]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad de Ciencias Médicas  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Costa Rica</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad de Ciencias Médicas  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Costa Rica</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2018</year>
</pub-date>
<volume>35</volume>
<numero>1</numero>
<fpage>3</fpage>
<lpage>10</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S1409-00152018000100003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S1409-00152018000100003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S1409-00152018000100003&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El cáncer de páncreas es una enfermedad mortal, principalmente porque se descubre muy tarde y es muy resistente a la quimioterapia y radioterapia. El tipo más común de cáncer de páncreas (más del 90%) se desarrolla a partir de las células exocrinas del páncreas y se denomina adenocarcinoma ductal pancreático (ACDP). Se han reconocido tres lesiones precursoras de cáncer de páncreas ductal: neoplasia intraepitelial pancreática (PanIN), neoplasia papilar-mucinosa intraductal (NPMI) y neoplasia quística mucinosa (NCM). Uno de los primeros eventos genéticos implicados en la patogénesis de ACDP es una mutación en el punto de activación en el oncogén KRAS, una mutación conductora oncogénica que se encuentra en más del 90% de todos los cánceres de páncreas. Además, se ha informado que hasta un 10% de los cánceres de páncreas están asociados con el historial familiar. Aunque la causa es multifactorial, el tabaquismo y la historia familiar son dominantes. Existe heterogeneidad morfológica en muchos cánceres humanos, pero parece ser un hallazgo particularmente común en ACDP. La cirugía solo es posible en 15-20% de los casos: tumores confinados al páncreas con posible afectación ganglionar local no muy extensa y que no produce afectación vascular o está limitada.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Pancreatic cancer is a deadly disease, mainly because it is generally discovered very late and it is very resistant to chemotherapy and radiation therapy. The most common type of pancreatic cancer (over 90%) develops from the exocrine cells of the pancreas and is named pancreatic ductal adenocarcinoma (PDAC). Three precursor lesions of ductal pancreatic cancer have been recognized: pancreatic intraepithelial neoplasia (PanIN), intraductal papillary-mucinous neoplasm (IPMN) and mucinous cystic neoplasm (MCN). One of the earliest genetic events involved in PDAC pathogenesis is an activating point mutation in the KRAS oncogene, an oncogenic driver mutation found in more than 90% of all pancreatic cancer. In addition, it has been reported that up to 10% of pancreatic cancer is associated with family history. Although the cause is multifactorial, cigarette smoking and family history are dominant. Morphological heterogeneity exists in many human cancers, but seems to be a particularly common finding in PDAC. Surgery is only possible in 15-20% of cases: tumors confined to the pancreas with possible local nodal involvement not very extensive and that do not produce vascular involvement or is limited.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Cáncer de páncreas (PC)]]></kwd>
<kwd lng="es"><![CDATA[Predisposición genética]]></kwd>
<kwd lng="es"><![CDATA[Riesgo familiar]]></kwd>
<kwd lng="es"><![CDATA[Adenocarcinoma ductal pancreático (ACDP)]]></kwd>
<kwd lng="es"><![CDATA[Cáncer de páncreas familiar (CPF)]]></kwd>
<kwd lng="es"><![CDATA[KRAS]]></kwd>
<kwd lng="es"><![CDATA[Neoplasia intraepitelial pancreática (PanIN)]]></kwd>
<kwd lng="en"><![CDATA[Pancreatic cáncer]]></kwd>
<kwd lng="en"><![CDATA[Genetic susceptibility]]></kwd>
<kwd lng="en"><![CDATA[Familial risk]]></kwd>
<kwd lng="en"><![CDATA[Pathology Pancreatic ductal adenocarcinoma (PDAC)]]></kwd>
<kwd lng="en"><![CDATA[Familial pancreatic cancer (FPC)]]></kwd>
<kwd lng="en"><![CDATA[KRAS]]></kwd>
<kwd lng="en"><![CDATA[Neoplasia intraepitelial pancreática (PanIN)]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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