<?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>0121-0319</journal-id>
<journal-title><![CDATA[Medicas UIS]]></journal-title>
<abbrev-journal-title><![CDATA[Medicas UIS]]></abbrev-journal-title>
<issn>0121-0319</issn>
<publisher>
<publisher-name><![CDATA[Universidad Industrial de Santander]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0121-03192021000100004</article-id>
<article-id pub-id-type="doi">10.18273/revmed.v34n1-2021004</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Desbalances genómicos del locus 9p24.1 en pacientes argentinos con linfoma de Hodgkin clásico]]></article-title>
<article-title xml:lang="en"><![CDATA[Genomic imbalances at 9p24.1 locus in Argentine patients with classical Hodgkin lymphoma]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[García-Montenegro]]></surname>
<given-names><![CDATA[Mauro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Narbaitz]]></surname>
<given-names><![CDATA[Marina]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Metrebian]]></surname>
<given-names><![CDATA[María Fernanda]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pavlovsky]]></surname>
<given-names><![CDATA[Astrid]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Slavutsky]]></surname>
<given-names><![CDATA[Irma]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Médico. Servicio de Patología, Fundaleu, Buenos Aires, Argentina. Servicio de Patología, Instituto de Investigaciones Hematológicas Mariano Castex, Academia Nacional de Medicina  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Argentina</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Médico. Servicio de Patología, Fundaleu, Buenos Aires, Argentina. Servicio de Patología, Instituto de Investigaciones Hematológicas Mariano Castex, Academia Nacional de Medicina  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Argentina</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Médico, Servicio de Patología, Instituto de Investigaciones Hematológicas Mariano Castex, Academia Nacional de Medicina  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Argentina</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Médico. Servicio de Hematología. Fundaleu  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Argentina</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,Dra. en Medicina. Laboratorio de Genética de Neoplasias Linfoides, Instituto de Medicina Experimental, CONICET - Academia Nacional de Medicina  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Argentina</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>04</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>04</month>
<year>2021</year>
</pub-date>
<volume>34</volume>
<numero>1</numero>
<fpage>35</fpage>
<lpage>44</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0121-03192021000100004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0121-03192021000100004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0121-03192021000100004&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción: El linfoma de Hodgkin clásico presenta escasas células de Reed Sternberg/Hodgkin inmersas en un abundante microambiente tumoral. Los desbalances genómicos del locus 9p24.1 han sido asociados con alteraciones en la expresión de los genes del ligando de muerte celular 1 y 2, ambos reguladores de la respuesta inmune.  Objetivo: Evaluar desbalances genómicos del locus 9p24.1 en células de Reed Sternberg/Hodgkin y del microambiente tumoral en biopsias de pacientes con linfoma de Hodgkin clásico y correlacionarlo con la expresión del ligando de muerte celular 1 y la presentación de la enfermedad.  Materiales y Métodos: Se efectuó hibridación in situ en biopsias de 22 pacientes con linfoma de Hodgkin clásico dirigida a los genes del ligando de muerte celular 1 y 2. Las alteraciones se clasificaron en: amplificación, ganancia y polisomía. La expresión se evaluó mediante inmunohistoquímica.  Resultados: Todos los pacientes mostraron alteraciones del número de copias. Se diferenciaron dos grupos: con amplificación (32%) y sin amplificación (68%); este último subdividido en: rico en ganancia (53%) y rico en polisomías (47%). El grupo rico en polisomías mostró mayor edad (p=0,027). El 40% de los pacientes con amplificación y rico en ganancias no presentó masa bulky. La expresión proteica mostró score +3 sólo en estos últimos. El title% de los casos ricos en polisomías presentaron monosomía del cromosoma 9 en los linfocitos circundantes respecto al 36,4% de los otros dos grupos.  Conclusiones: Nuestros datos constituyen un aporte a la caracterización biológica del LHC, de interés en el marco de las nuevas modalidades terapéuticas. MÉD.UIS.2020;34(1):35-44.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Background: Classical Hodgkin lymphoma shows scarce tumor Reed-Sternberg/Hodgkin cells surrounded by a dense immune microenvironment. Genetic alterations at the 9p24.1 locus result in genomic imbalances in the copy number of PD-L1/PD-L2 genes, both of them being immune response regulators.  Aim: To characterize genomic imbalances at the 9p24.1 locus in Reed-Sternberg/Hodgkin cells and immune microenvironment in biopsies of patients with Classical Hodgkin lymphoma and correlate it with PD-L1 protein expression and disease presentation.  Material and Methods: Paraffin embedded biopsies of 22 patients with CHL were retrospectively evaluated by fluorescence in situ hybridization using SPEC CD274/PDCD1LG2/CEN9 DNA probe. The frequency of 9p24.1 alterations, amplification, copy gain and polysomy, were determined taking into account the number of gene copies with respect to the centromere. PD-L1 protein expression was evaluated by immunohistochemistry.  Results: All cases presented alterations in the number of copies of PD-L1 / PD-L2, which are differentiated in two groups: with amplification (32%) and without amplification (68%). The latter was subdivided into rich in gains (RG) (53%) and rich in polysomies (RP) (47%). Groups with amplification and RG were younger than the RP group (p = 0.027). The latter was not associated with bulky disease, a fact observed in 40% of patients with amplification and RG. Protein expression showed score +3 only in the latter. All RP cases presented chromosome 9 monosomy in the surrounding lymphocytes, compared to 36.4% of the other two groups.  Conclusions: Our data contributes to the biologic characterization of CHL, of interest in the context of new therapeutic modalities. MÉD.UIS.2020;34(1):35-44]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Linfoma de Hodgkin]]></kwd>
<kwd lng="es"><![CDATA[FISH; PD-L1/PD-L2 (Programmed cell death ligand 1/2)]]></kwd>
<kwd lng="es"><![CDATA[Expresión génica]]></kwd>
<kwd lng="en"><![CDATA[Hodgkin lymphoma]]></kwd>
<kwd lng="en"><![CDATA[FISH; PD-L1/PD-L2 (Programmed cell death ligand 1-2)]]></kwd>
<kwd lng="en"><![CDATA[Gene expression]]></kwd>
</kwd-group>
</article-meta>
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