<?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>2007-8447</journal-id>
<journal-title><![CDATA[Revista biomédica]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. biomédica]]></abbrev-journal-title>
<issn>2007-8447</issn>
<publisher>
<publisher-name><![CDATA[Universidad Autónoma de Yucatán, Centro de Investigaciones Regionales Dr. Hideyo Noguchi Naturaleza]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2007-84472018000300071</article-id>
<article-id pub-id-type="doi">10.32776/revbiomed.v29i3.622</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Determinación de mutaciones (del E746-A750 exón 19 y L858R exón 21) en el gen receptor del factor de crecimiento epidérmico (EGFR) en muestras de suero y biopsia de carcinoma pulmonar no microcítico (CPNM)]]></article-title>
<article-title xml:lang="en"><![CDATA[Determination of mutations (del E746-A750 exon 19 and L858R exon 21) in the epidermal growth factor receptor (EGFR) gene in serum samples and in biopsys of non-microcytic lung carcinoma (NMLC)]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Castro-Valencia]]></surname>
<given-names><![CDATA[Karla]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González-Herrera]]></surname>
<given-names><![CDATA[Lizbeth]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Muñoz-Santos]]></surname>
<given-names><![CDATA[Elena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-González]]></surname>
<given-names><![CDATA[Paola]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sosa-Escalante]]></surname>
<given-names><![CDATA[Javier Enrique]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Mendoza]]></surname>
<given-names><![CDATA[Gerardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Medina-Escobedo]]></surname>
<given-names><![CDATA[Gilberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Autónoma de Yucatán. Mérida Centro de Investigaciones Regionales &#8220;Dr. Hideyo Noguchi&#8221; Laboratorio de Genética]]></institution>
<addr-line><![CDATA[ Yucatán]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,DIMYGEN Laboratorio S.C.P.  ]]></institution>
<addr-line><![CDATA[Mérida Yucatán]]></addr-line>
<country>México</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Instituto Mexicano del Seguro Social Unidad Médica de alta especialidad del Centro Médico Nacional &#8220;Dr. Ignacio García Téllez&#8221; Departamento de Patología]]></institution>
<addr-line><![CDATA[Mérida Yucatán]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2018</year>
</pub-date>
<volume>29</volume>
<numero>3</numero>
<fpage>71</fpage>
<lpage>79</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2007-84472018000300071&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2007-84472018000300071&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2007-84472018000300071&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción Las mutaciones, del E746-A750 exón 19 y L858R exón 21 del gen EGFR en células tumorales de CPNM representan biomarcadores de respuesta a fármacos inhibidores de tirosina cinasa (ITK). Pacientes con tumores positivos a mutaciones EGFR muestran mejor respuesta y mayor sobrevivencia. Estas mutaciones ocupan el 90% de las mutaciones en cáncer de pulmón.  Objetivo Evaluar la frecuencia de las mutaciones del E746-A750 exón 19 y L858R exón 21 del EGFR en muestras de biopsia de CPNM y en muestras de suero de población abierta de Yucatán.  Material y métodos Se seleccionaron 19 muestras de biopsia de CNPM tipo adeconocarcinoma y 101 sueros de sujetos sanos. Las mutaciones del E746-A750 y L858R en EGFR se determinaron mediante amplificación por PCR oligo-alelo específica (PCR-ASO). Se calcularon las frecuencias genotípicas y alélicas y su distribución según Hardy Weinberg, utilizando la plataforma SNPstats.  Resultados En muestras de suero se determinó el genotipo homocigoto (1/1) en 26.58%, 73.42% el heterocigoto (1/0) y ausencia del genotipo mutante con deleción (0/0) para del E746-A750; en tanto que, para L858R, 21.78% resultó homocigoto (TT), 54.46% heterocigoto (T/G) y 23.76% mutantes GG. En las biopsias, el heterocigoto fue más frecuente en ambas mutaciones 63.16% y 73.68% para del E746-A750 y L858R, respectivamente.  Conclusión. La frecuencia de las mutaciones del gen EGFR en las muestras de sueros fue de 36.71% para la deleción del E746-A750 en exón 19 y 50.99% para L858R en exón 21. La distribución de las mutaciones en muestras de biopsia CPNM resultó en 42.11% para cada mutación estudiada.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction EGFR mutations, del E746-A750 in exon 19 and L858R in exon 21 in tumor cells of NMLC represent biomarkers of response to tyrosine kinase inhibitors (TKI) therapy. Patients with tumors positive for EGFR mutations show better response and greater survival. These mutations occupy 90% of mutations in lung cancer.  Objective To evaluate the frequency of mutations del E746-A750-exon 19 and L858R-exon 21 of EGFR gene in NMLC biopsy samples and in serum samples of the general population from Yucatán.  Material and methods 19 NMLC biopsy samples of adenocarcinoma type and 101 serum samples from healthy subjects were selected. EGFR mutations del E746-A750 and L858R were determined by allele-specific PCR amplification (PCR-ASO). The genotypic and allelic frequencies; and their distribution according to Hardy Weinberg expectations were calculated using the SNPstats software.  Results For serum, EGFR del E746-A750 mutation, homozygous genotype (1/1) was present in 26.58%, heterozygote (1/0) in 73.42% and absence of mutant genotype with deletion (0/0); whereas for L858R mutation, 21.78% were homozygous (TT), 54.46% heterozygous (T/G) and 23.76% GG mutants. For the NMLC biopsies, the heterozygote was the most frequent genotype for both mutations, 63.16% and 73.68% for del E746-A750 and L858R, respectively.  Conclusion The frequency of mutations of EGFR gene in serum samples was 36.71% for deletion delE746-A750 in exon 19 and 50.99% for L858R in exon 21. Distribution of mutations in biopsy samples NMLC resulted in 42.11% for each EGFR mutation.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Mutación EGFR]]></kwd>
<kwd lng="es"><![CDATA[cáncer de pulmón]]></kwd>
<kwd lng="es"><![CDATA[inhibidores de tirosina cinasa]]></kwd>
<kwd lng="en"><![CDATA[EGFR mutation]]></kwd>
<kwd lng="en"><![CDATA[lung cancer]]></kwd>
<kwd lng="en"><![CDATA[thyrosine kinase inhibitors ITK]]></kwd>
</kwd-group>
</article-meta>
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