<?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>S1665-11462020000400186</article-id>
<article-id pub-id-type="doi">10.24875/bmhim.19000187</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Yin-Yang-1 decreases Fas-induced apoptosis in acute lymphoblastic leukemia under hypoxic conditions: its implications in immune evasion]]></article-title>
<article-title xml:lang="es"><![CDATA[YY1 induce la disminución de la apoptosis a través de Fas en la leucemia linfoblástica aguda en condiciones hipóxicas: implicaciones en la evasión de la respuesta inmunitaria]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Martínez-Torres]]></surname>
<given-names><![CDATA[Estefany]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-Pérez]]></surname>
<given-names><![CDATA[Tania V.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Morales-Martínez]]></surname>
<given-names><![CDATA[Mario]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Huerta-Yepez]]></surname>
<given-names><![CDATA[Sara]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez Unidad de Investigación en Enfermedades Oncológicas ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez Unidad de Investigación en Enfermedades Oncológicas ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Instituto Mexicano del Seguro Social Hospital de Oncología Laboratorio de Señalización Molecular en Cáncer Molecular]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Instituto Mexicano del Seguro Social Centro Médico Nacional de México Siglo XXI ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>08</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>08</month>
<year>2020</year>
</pub-date>
<volume>77</volume>
<numero>4</numero>
<fpage>186</fpage>
<lpage>194</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-11462020000400186&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-11462020000400186&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-11462020000400186&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Background: Acute lymphoblastic leukemia (ALL) is an aggressive malignant disease with high prevalence in pediatric patients. It has been shown that the downregulation of Fas expression is correlated with an inadequate response in ALL, although these mechanisms are still not well understood. Several reports demonstrated that hypoxia is involved in dysfunctional apoptosis. Yin-Yang-1 (YY1) transcription factor is involved in resistance to apoptosis, tumor progression, and it is increased in different types of cancer, including leukemia. The regulatory mechanism underlying YY1 expression in leukemia is still not understood, but it is known that YY1 negatively regulates Fas expression. The study aimed to evaluate the effect of YY1 on Fas expression under hypoxic conditions in ALL.  Methods: Leukemia cell line RS4; 11 was cultured under normoxic and hypoxic conditions. YY1, Fas receptor, and hypoxia-inducible factor (HIF-1&#945;) expression were analyzed. After treatment with a Fas agonist (DX2), apoptosis was analyzed through the detection of active caspase 3. Data were analyzed using Pearson’s correlation.  Results: Leukemia cells co-expressed both HIF-1&#945; and YY1 under hypoxia, which correlated with a downregulation of Fas expression. During hypoxia, the levels of apoptosis diminished after DX2 treatment. The analysis revealed that patients with high levels of HIF-1&#945; also express high levels of YY1 and low levels of Fas.  Conclusions: These results suggest that YY1 negatively regulates the expression of the Fas receptor, which could be involved in the escape of leukemic cells from the immune response contributing to the ALL pathogenesis.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción: La leucemia linfoblástica aguda (LLA) es una enfermedad con alta prevalencia en la población pediátrica. El mecanismo por el cual el receptor de Fas participa en la regulación inmunitaria en los tumores es desconocido, pero se sabe que está subexpresado en LLA. El factor de transcripción Ying-Yang-1 (YY1) está involucrado en la resistencia a la apoptosis y la progresión tumoral; se encuentra aumentado en diferentes tumores, incluida la LLA. Aunque los mecanismos que regulan la expresión de YY1 en LLA son desconocidos, se sabe que YY1 regula la expresión del receptor de Fas. El objetivo de este trabajo fue evaluar el efecto de YY1 en la expresión de Fas en condiciones de hipoxia en la LLA.  Métodos: Se cultivaron células RS4;11 en condiciones de hipoxia y se analizó la expresión de YY1, receptor de Fas y HIF-1&#945;. La apoptosis fue inducida usando un agonista de Fas (DX2) y se analizó con la detección de caspasa 3 activa. Los datos se analizaron mediante correlación de Pearson.  Resultados: Las células RS4;11 coexpresaron HIF-1&#945;y YY1 en hipoxia, lo cual correlaciona con una baja expresión de Fas. La apoptosis se encontró disminuida durante condiciones de hipoxia, después del tratamiento con DX2. El análisis bioinformático mostró que los pacientes con altos niveles de HIF-1&#945;presentan YY1 elevado y bajos niveles del receptor de Fas.  Conclusiones: Estos resultados sugieren que YY1 regula negativamente la expresión del receptor de Fas, lo cual podría estar involucrado en el escape de las células leucémicas a la respuesta inmunitaria, contribuyendo a la patogénesis de la LLA.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Yin-Yang-1]]></kwd>
<kwd lng="en"><![CDATA[Fas]]></kwd>
<kwd lng="en"><![CDATA[Hypoxia-inducible factor-1&#945;]]></kwd>
<kwd lng="en"><![CDATA[Hypoxia]]></kwd>
<kwd lng="en"><![CDATA[Acute lymphoblastic leukemia]]></kwd>
<kwd lng="es"><![CDATA[YY1]]></kwd>
<kwd lng="es"><![CDATA[Fas]]></kwd>
<kwd lng="es"><![CDATA[HIF-1&#945;]]></kwd>
<kwd lng="es"><![CDATA[Hipoxia]]></kwd>
<kwd lng="es"><![CDATA[Leucemia linfoblástica aguda]]></kwd>
</kwd-group>
</article-meta>
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