<?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>1665-1146</journal-id>
<journal-title><![CDATA[Boletín médico del Hospital Infantil de México]]></journal-title>
<abbrev-journal-title><![CDATA[Bol. Med. Hosp. Infant. Mex.]]></abbrev-journal-title>
<issn>1665-1146</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Salud, Hospital Infantil de México Federico Gómez]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1665-11462017000400243</article-id>
<article-id pub-id-type="doi">10.1016/j.bmhimx.2017.02.005</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Alteraciones epigenéticas en leucemia linfoblástica aguda]]></article-title>
<article-title xml:lang="en"><![CDATA[Epigenetic alterations in acute lymphoblastic leukemia]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Navarrete-Meneses]]></surname>
<given-names><![CDATA[María del Pilar]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Vera]]></surname>
<given-names><![CDATA[Patricia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Nacional de Pediatría  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>08</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>08</month>
<year>2017</year>
</pub-date>
<volume>74</volume>
<numero>4</numero>
<fpage>243</fpage>
<lpage>264</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-11462017000400243&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-11462017000400243&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-11462017000400243&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: La leucemia linfoblástica aguda (LLA) es el tipo de cáncer más frecuente en niños. Aunque se sabe que las alteraciones genéticas constituyen la base de la etiología de la LLA, se ha demostrado que no son suficientes para el desarrollo leucémico; son necesarias alteraciones adicionales, como las modificaciones epigenéticas. En la LLA se han identificado alteraciones de este tipo, como la metilación del DNA, la modificación de histonas y la regulación por RNAs no codificantes. La hipermetilación del DNA en regiones promotoras es una de las alteraciones epigenéticas más frecuentes en LLA: y conlleva al silenciamiento de genes que generalmente son supresores de tumor y, en consecuencia, contribuye a la leucemogénesis. También se han detectado alteraciones en proteínas remodeladoras de histonas, como la sobreexpresión de enzimas desacetilasas de histonas, así como alteraciones en enzimas acetil transferasas y metil transferasas. En la LLA también se altera la expresión de miRNAs, lo cual produce desregulación en la expresión de sus genes blanco. Estas modificaciones epigenéticas son eventos clave en la transformación maligna, e involucran la desregulación de oncogenes como BLK, WNT5B y WISP1 y de supresores de tumor como FHIT, CDKN2A, CDKN2B y TP73, lo que afecta diversos procesos celulares fundamentales que conllevan al desarrollo de LLA. Las alteraciones epigenéticas y genéticas contribuyen en conjunto al desarrollo y evolución de la LLA.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. It is well-known that genetic alterations constitute the basis for the etiology of ALL. However, genetic abnormalities are not enough for the complete development of the disease, and additional alterations such as epigenetic modifications are required. Such alterations, like DNA methylation, histone modifications, and noncoding RNA regulation have been identified in ALL. DNA hypermethylation in promoter regions is one of the most frequent epigenetic modifications observed in ALL. This modification frequently leads to gene silencing in tumor suppressor genes, and in consequence, contributes to leukemogenesis. Alterations in histone remodeling proteins have also been detected in ALL, such as the overexpression of histone deacetylases enzymes, and alteration of acetyltransferases and methyltransferases. ALL also shows alteration in the expression of miRNAs, and in consequence, the modification in the expression of their target genes. All of these epigenetic modifications are key events in the malignant transformation since they lead to the deregulation of oncogenes as BLK, WNT5B and WISP1, and tumor suppressors such as FHIT, CDKN2A, CDKN2B, and TP53, which alter fundamental cellular processes and potentially lead to the development of ALL. Both genetic and epigenetic alterations contribute to the development and evolution of ALL.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Leucemia linfoblástica aguda]]></kwd>
<kwd lng="es"><![CDATA[Epigenética]]></kwd>
<kwd lng="es"><![CDATA[Expresión génica]]></kwd>
<kwd lng="es"><![CDATA[Metilación del DNA]]></kwd>
<kwd lng="es"><![CDATA[Modificaciones de histonas]]></kwd>
<kwd lng="es"><![CDATA[miRNAs]]></kwd>
<kwd lng="en"><![CDATA[Acute lymphoblastic leukemia]]></kwd>
<kwd lng="en"><![CDATA[Epigenetics]]></kwd>
<kwd lng="en"><![CDATA[Gene expression]]></kwd>
<kwd lng="en"><![CDATA[DNA methylation]]></kwd>
<kwd lng="en"><![CDATA[Histone modifications]]></kwd>
<kwd lng="en"><![CDATA[miRNAs]]></kwd>
</kwd-group>
</article-meta>
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