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Chromosome 14q may harbor multiple tumor suppressor genes in primary glioblastoma multiforme / 中华医学杂志(英文版)
Chinese Medical Journal ; (24): 1201-1204, 2002.
Artigo em Inglês | WPRIM | ID: wpr-340357
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate whether deletion of chromosome 14q is involved in the carcinogenesis of primary glioblastoma multiforme and to identify possibly common deletion regions. METHJODS Fourteen fluorescent dye-labeled polymorphic markers were used and polymerase chain reaction-based microsatellite analysis was employed to investigate loss of heterozygosity (LOH) on chromosome 14q in 20 primary glioblastoma multiforme (GBM).</p><p><b>RESULTS</b>Ten of twenty (50%) GBM displayed LOH at one or more of the markers on chromosome 14q. Five tumors showed either LOH or non-informative on all markers tested. The most frequent LOH was observed at locus D14S65 (57.1%) on 14q32.1, and in the chromosomal region spanning from D14S63 (47.1%) to D14S74 (46.7%) on 14q23-31. None of the informative loci exhibited microsatellite instability.</p><p><b>CONCLUSIONS</b>Allelic deletion on chromosome 14q plays an important role in the pathogenesis of GBM. Chromosomal regions at locus D14S65 on 14q32.1 and spanning from D14S63 to D14S74 on 14q23-31 may harbor multiple tumor suppressor genes associated with GBM.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Cromossomos Humanos Par 14 / Genes Supressores de Tumor / Glioblastoma / Repetições de Microssatélites / Perda de Heterozigosidade / Genética Limite: Adulto / Idoso / Feminino / Humanos / Masculino Idioma: Inglês Revista: Chinese Medical Journal Ano de publicação: 2002 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Cromossomos Humanos Par 14 / Genes Supressores de Tumor / Glioblastoma / Repetições de Microssatélites / Perda de Heterozigosidade / Genética Limite: Adulto / Idoso / Feminino / Humanos / Masculino Idioma: Inglês Revista: Chinese Medical Journal Ano de publicação: 2002 Tipo de documento: Artigo