<?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>0864-0289</journal-id>
<journal-title><![CDATA[Revista Cubana de Hematología, Inmunología y Hemoterapia]]></journal-title>
<abbrev-journal-title><![CDATA[Rev Cubana Hematol Inmunol Hemoter]]></abbrev-journal-title>
<issn>0864-0289</issn>
<publisher>
<publisher-name><![CDATA[Centro Nacional de Información de Ciencias MédicasEditorial Ciencias Médicas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0864-02892020000100009</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Casos atípicos e14a3 (b3a3) en el gen de fusión BCR-ABL de la leucemia mieloide crónica en Cuba]]></article-title>
<article-title xml:lang="en"><![CDATA[Rare cases of e14a3 (b3a3) BCR-ABL fusion in chronic myeloid leukemia in Cuba]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ruiz Moleón]]></surname>
<given-names><![CDATA[Vera]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Díaz Alonso]]></surname>
<given-names><![CDATA[Carmen Alina]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Amor Vigil]]></surname>
<given-names><![CDATA[Ana María]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Fernández Martínez]]></surname>
<given-names><![CDATA[Lesbia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Garrote Santana]]></surname>
<given-names><![CDATA[Heidys]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto de Hematología e Inmunología  ]]></institution>
<addr-line><![CDATA[La Habana ]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<volume>36</volume>
<numero>1</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_arttext&amp;pid=S0864-02892020000100009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_abstract&amp;pid=S0864-02892020000100009&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_pdf&amp;pid=S0864-02892020000100009&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Introducción:  La leucemia mieloide crónica es un desorden clonal maligno de células madres hematopoyéticas pluripotentes que se caracteriza por la presencia del cromosoma Filadelfia, consecuencia de la traslocación cromosómica recíproca entre los brazos largos de los cromosomas 9 y 22. El resultado de esta alteración cromosómica es un gen de fusión que contiene las uniones b2a2 (e13a2) o b3a2 (e14a2). En la mayor parte de los casos, las células de la leucemia mieloide crónica expresan uno de los dos transcritos (b2a2 o b3a2); sin embargo, el 5 % de los pacientes tienen ambos tipos de ARNm como resultado de empalmes alternativos. Se han encontrado otros transcriptos como e19a2, e2a2, e1a3, e6a2, e13a3(b2a3), y e14a3(b3a3), que ocurren con menos frecuencia.  Objetivo:  Describir el comportamiento de dos pacientes con leucemia mieloide crónica que presentan un trascripto BCR/ABL atípico.  Casos clínicos:  En el estudio molecular por reacción en cadena de la polimerasa cualitativo realizado a los dos pacientes, se observó un punto de ruptura del gen de fusión BCR/ABL poco frecuente, el cual se correspondía al transcripto e14a3 (b3a3). Estos pacientes iniciaron tratamiento con mesilato de imatinib a dosis de 400 mg diarios. Al primer paciente a los dos meses de tratamiento se le detectó crisis blástica, por lo que se le cambió el tratamiento a nilotinib 400 mg diarios que mantiene hasta la actualidad. La segunda paciente mantuvo igual tratamiento, aunque en ocasiones ha sido necesario incorporar tratamiento citorreductor con hidroxiurea por presentar leucocitosis.  Conclusiones:  Los pacientes con BCR/ABL a3 presentan un curso más benigno de la enfermedad. Aunque en los pacientes estudiados no se observó una respuesta satisfactoria al tratamiento pues presentaron diversas complicaciones.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT  Introduction:  Chronic myeloid leukemia is a malignant clonal disorder of pluripotent hematopoietic stem cells and characterized by the presence of the Philadelphia chromosome, which is the product of a reciprocal translocation between the long arms of chromosomes 9 and 22. The result of this chromosomal alteration is a fusion gene that contains the e13a2 (b2a2) and e14a2 (b3a2) junctions. In most cases, chronic myeloid leukemia cells express one of the two transcripts (b2a2 or b3a2); however, 5% of patients have both types of mRNA, as a result of alternative junctions. Other transcripts have been identified, such as e19a2, e2a2, e1a3, e6a2, e13a3 (b2a3), and e14a3 (b3a3), which occur less frequently.  Objective: To describe the behavior of two patients with chronic myeloid leukemia who have an atypical BCR-ABL transcript.  Clinical cases:  In a qualitative molecular study of polymerase chain reaction carried out with two patients, a BCR-ABL fusion gene breakpoint was observed, which corresponded to the e14a3 (b3a3) transcript. These patients started treatment with imatinib mesylate at a dose of 400mg/d. At two months, the first patient had a diagnose of blast crisis, so the treatment was changed to nilotinib at a dose of 400mg/d, which the patient maintained to date. The second patient maintained the same treatment, although it was sometimes necessary to incorporate cytoreductive treatment with hydroxyurea due to leukocytosis.  Conclusions:  Patients with BCR-ABL a3 present a more benign evolution of the disease. However, a satisfactory response to treatment was not observed in the patients studied, as long as they presented various complications.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[leucemia mieloide crónica]]></kwd>
<kwd lng="es"><![CDATA[gen de fusión BCR/ABL]]></kwd>
<kwd lng="es"><![CDATA[transcriptos e14a3 y b3a3]]></kwd>
<kwd lng="es"><![CDATA[puntos de ruptura]]></kwd>
<kwd lng="en"><![CDATA[chronic myeloid leukemia]]></kwd>
<kwd lng="en"><![CDATA[BCR-ABL fusion gene]]></kwd>
<kwd lng="en"><![CDATA[transcripts e14a3 and b3a3]]></kwd>
<kwd lng="en"><![CDATA[breakpoints]]></kwd>
</kwd-group>
</article-meta>
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