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        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">El an&#225;lisis citogen&#233;tico y molecular de los tumores del Sistema Nervioso ha proporcionado en los &#250;ltimos a&#241;os una informaci&#243;n primordial acerca de los mecanismos responsables de su origen y desarrollo&#46; As&#237; por ejemplo&#44; sabemos que los gliomas muestran un patr&#243;n complejo de afectaci&#243;n cromos&#243;mica que generalmente implica&#58; ganancia de cromosomas del par 7 y p&#233;rdidas proporcionales de los cromosomas o regiones cromos&#243;micas 1p&#44; 9p&#44; 10&#44; 17p&#44; 19q y 22q&#46; La caracterizaci&#243;n molecular de estas anomal&#237;as ha demostrado que las mutaciones del gen TP53 junto con la p&#233;rdida de alelos a nivel de 17p podr&#237;an acontecer en etapas tempranas del desarrollo de estos tumores&#44; mientras que las alteraciones a nivel de los cromosomas 13 y 22&#44; aunque acontecimientos tempranos&#44; s&#243;lo caracterizar&#237;an determinados subtipos de gliomas&#44; del mismo modo que las alterciones de 1p y 19q contribuyen preferentemente al desarrollo de oligodendrogliomas&#46; La p&#233;rdida de secuencias gen&#243;micas a nivel de los cromosomas 10 y 9p &#40;es decir de un gen oncosupresor localizado en dichos cromosomas&#41; y la amplificaci&#243;n del gen codificador del receptor del factor de crecimiento epid&#233;rmico &#40;EGFR&#41; parecen ser anomal&#237;as que&#44; de forma secuencial&#44; contribuyen a la g&#233;nesis de las formas tumorales de mayor grado de malignidad&#58; Astrocitoma anapl&#225;sico y Glioblastoma multiforme&#46; Los datos disponibles en relaci&#243;n a Meningiomas y Neurinomas han demostrado que la p&#233;rdida de material gen&#233;tico a nivel del cromosoma 22 representa un factor primordial para su desarrollo&#46; Seg&#250;n esto&#44; un gen o genes de car&#225;cter oncosupresor&#44; localizados en este cromosoma&#44; participar&#237;an en la g&#233;nesis de ambas neoplasias&#44; cuya forma de presentaci&#243;n puede ser como tumores espor&#225;dicos o asociados a la neurofibromatosis de tipo 2 &#40;NF-2&#41;&#46; El an&#225;lisis molecular de amplias series de meningiomas muestra que la regi&#243;n perdida corresponder&#237;a a la porci&#243;n distal del cromosoma&#44; mientras que recientemente se ha aislado un gen responsable del desarrollo de NF-2&#44; cuya localizaci&#243;n ser&#237;a m&#225;s proximal&#46; Estos datos indican que dos o hasta tres genes diferentes parecen participar de forma activa en la carcinogenesis de los tumores de origen nervioso&#58; a&#46; gen NF-2 localizado a nivel de 22q12&#44; que potencialmente desempe&#241;a alg&#250;n papel en el desarrollo de neurinomas y de ciertos meningiomas&#59; b&#46; locus de meningioma&#44; situado a nivel de 22q12&#46;3-qter&#44; que contribuir&#237;a de forma espec&#237;fica en la genesis de meningiomas&#59; c&#46; locus de gliomas&#44; a nivel de 22q13&#46;2-qter&#44; cuya participaci&#243;n parece espec&#237;fica en determinados subgrupos de gliomas&#46; Los trabajos encaminados a la identificaci&#243;n y aislamiento de todos los genes involucrados&#44; as&#237; como tambi&#233;n el an&#225;lisis funcional de sus productos proteicos&#44; contribuir&#225;n a obtener un mejor y m&#225;s exacto conocimiento de los factores desencadenantes del desarrollo de los tumores de origen nervioso&#44; con implicaciones cl&#237;nicas a nivel de diagn&#243;stico&#44; pron&#243;stico&#44; tratamiento&#44; etc&#46; de los pacientes afectos&#46;</p>"
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        "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Cytogenetic and molecular genetic analyses of the major histological subtypes of tumors of the Nervous System &#40;neurinomas&#44; meningiomas and gliomas&#41; have provided interesting data on the molecular mechanisms involved in their origin and development&#46; A complex pattern of chromosomal abnormalities has been identified in malignant gliomas&#44; including gains of chromosome 7 and losses of chromosomes 10&#44; 9p&#44; 17p&#44; and 22&#46; The molecular characterization of these abnormalities has demonstrated that anomalies of the TP53 gene&#44; and the loss of alleles at 17p seem to be the earliest abnormalities occurring during the genesis and progression of these neoplasms&#46; The loss of regions on chromosomes 13 and 22 might also represent early events&#44; perhaps characterizing subgroups of low grade tumors&#46; Data available on meningiomas and neurinomas show that loss of regions on chromosome 22 is the main cytogenetic feature&#46; Thus&#44; tumor suppressor genes located in this chromosome are non-randomly involved in both neoplasms&#46; The molecular studies in these tumor types have shown that loci placed at 22q12 or the gene responsible for the development of neurofibromatosis type 2&#44; also located here&#44; might be the target for the anomalies of chromosome 22&#44; detected in meningiomas or neurinomas&#46; Efforts to identify and isolate the genes involved in these neoplasms will contribute to a better understanding of the mechanisms of oncogenesis in brain tumors and will doubtless have a clinical impact on the diagnosis&#44; treatment and prognosis of the patients&#46;</p>"
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Vol. 5. Núm. 3.
Páginas 183-193 (enero 1993)
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Vol. 5. Núm. 3.
Páginas 183-193 (enero 1993)
Citogenética y genética molecular de tumores del sistema nervioso
Visitas
1907
M.J. Bello, J.A. Rey
Instituto de Investigaciones Biomédicas del CSIC. Madrid
J.M. de Campos*, M.E. Kusak**, J. Vaquero***
* Servicios de Neurocirugía de. Clínica Puerta de Hierro. Madrid
** Fundación Jiménez Díaz. Clínica Puerta de Hierro. Madrid
*** Hospital de laPrincesa, y Clínica Puerta de Hierro. Madrid
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El análisis citogenético y molecular de los tumores del Sistema Nervioso ha proporcionado en los últimos años una información primordial acerca de los mecanismos responsables de su origen y desarrollo. Así por ejemplo, sabemos que los gliomas muestran un patrón complejo de afectación cromosómica que generalmente implica: ganancia de cromosomas del par 7 y pérdidas proporcionales de los cromosomas o regiones cromosómicas 1p, 9p, 10, 17p, 19q y 22q. La caracterización molecular de estas anomalías ha demostrado que las mutaciones del gen TP53 junto con la pérdida de alelos a nivel de 17p podrían acontecer en etapas tempranas del desarrollo de estos tumores, mientras que las alteraciones a nivel de los cromosomas 13 y 22, aunque acontecimientos tempranos, sólo caracterizarían determinados subtipos de gliomas, del mismo modo que las alterciones de 1p y 19q contribuyen preferentemente al desarrollo de oligodendrogliomas. La pérdida de secuencias genómicas a nivel de los cromosomas 10 y 9p (es decir de un gen oncosupresor localizado en dichos cromosomas) y la amplificación del gen codificador del receptor del factor de crecimiento epidérmico (EGFR) parecen ser anomalías que, de forma secuencial, contribuyen a la génesis de las formas tumorales de mayor grado de malignidad: Astrocitoma anaplásico y Glioblastoma multiforme. Los datos disponibles en relación a Meningiomas y Neurinomas han demostrado que la pérdida de material genético a nivel del cromosoma 22 representa un factor primordial para su desarrollo. Según esto, un gen o genes de carácter oncosupresor, localizados en este cromosoma, participarían en la génesis de ambas neoplasias, cuya forma de presentación puede ser como tumores esporádicos o asociados a la neurofibromatosis de tipo 2 (NF-2). El análisis molecular de amplias series de meningiomas muestra que la región perdida correspondería a la porción distal del cromosoma, mientras que recientemente se ha aislado un gen responsable del desarrollo de NF-2, cuya localización sería más proximal. Estos datos indican que dos o hasta tres genes diferentes parecen participar de forma activa en la carcinogenesis de los tumores de origen nervioso: a. gen NF-2 localizado a nivel de 22q12, que potencialmente desempeña algún papel en el desarrollo de neurinomas y de ciertos meningiomas; b. locus de meningioma, situado a nivel de 22q12.3-qter, que contribuiría de forma específica en la genesis de meningiomas; c. locus de gliomas, a nivel de 22q13.2-qter, cuya participación parece específica en determinados subgrupos de gliomas. Los trabajos encaminados a la identificación y aislamiento de todos los genes involucrados, así como también el análisis funcional de sus productos proteicos, contribuirán a obtener un mejor y más exacto conocimiento de los factores desencadenantes del desarrollo de los tumores de origen nervioso, con implicaciones clínicas a nivel de diagnóstico, pronóstico, tratamiento, etc. de los pacientes afectos.

Palabras clave:
Citogenética
Genética molecular
Oncogenes
Genes oncosupresores
Tumores del sistema nervioso
Glioma
Meningioma
Neurinoma
Summary

Cytogenetic and molecular genetic analyses of the major histological subtypes of tumors of the Nervous System (neurinomas, meningiomas and gliomas) have provided interesting data on the molecular mechanisms involved in their origin and development. A complex pattern of chromosomal abnormalities has been identified in malignant gliomas, including gains of chromosome 7 and losses of chromosomes 10, 9p, 17p, and 22. The molecular characterization of these abnormalities has demonstrated that anomalies of the TP53 gene, and the loss of alleles at 17p seem to be the earliest abnormalities occurring during the genesis and progression of these neoplasms. The loss of regions on chromosomes 13 and 22 might also represent early events, perhaps characterizing subgroups of low grade tumors. Data available on meningiomas and neurinomas show that loss of regions on chromosome 22 is the main cytogenetic feature. Thus, tumor suppressor genes located in this chromosome are non-randomly involved in both neoplasms. The molecular studies in these tumor types have shown that loci placed at 22q12 or the gene responsible for the development of neurofibromatosis type 2, also located here, might be the target for the anomalies of chromosome 22, detected in meningiomas or neurinomas. Efforts to identify and isolate the genes involved in these neoplasms will contribute to a better understanding of the mechanisms of oncogenesis in brain tumors and will doubtless have a clinical impact on the diagnosis, treatment and prognosis of the patients.

Key words:
Cytogenetics
Molecular genetics
Oncogenes
Tumor suppressor genes
Nervous system tumors
Brain tumors
Glioma
Meningioma
Neurinoma

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