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Provedor de dados:  Genet. Mol. Biol.
País:  Brazil
Título:  Enhanced levels of the apoptotic BAX/BCL-2 ratio in children with acute lymphoblastic leukemia and high-risk features
Autores:  Kaparou,Maria
Choumerianou,Despoina
Perdikogianni,Chrysoula
Martimianaki,Georgia
Kalmanti,Maria
Stiakaki,Eftichia
Data:  2013-01-01
Ano:  2013
Palavras-chave:  Leukemia
Real-time PCR analysis
Protein
Resumo:  It has been suggested that leukemia is characterized by an impaired balance between the proliferation of blood cells and their capacity to undergo apoptosis. The aim of this study was to examine the expression of key molecules related to apoptosis (BCL-2, BAX, FAS, FAS-L) in children with acute lymphoblastic leukemia (ALL). Measurement of BCL-2 and BAX mRNA was performed by quantitative real-time PCR, and membrane expression of FAS and FAS-L was assessed by flow cytometry in bone marrow mononuclear cells, both at diagnosis and at remission following induction chemotherapy. At diagnosis, increased levels of the apoptotic BAX/BCL-2 ratio were observed in children older than 10 years and with higher white blood cell counts. A DNA index < 1.16 was associated with increased BAX/BCL-2, both at diagnosis and at remission, and the del(9p) chromosome abnormality with increased BAX/BCL-2 at remission. The expression of the apoptotic receptor FAS was significantly higher at remission compared to diagnosis, which might reflect enhanced sensitivity of the leukemic clone to apoptosis and response to treatment. Altogether, our results highlight the association of apoptosis-related genes with clinical and cytogenetic prognostic parameters in pediatric ALL. A better understanding of the mechanisms and regulation of apoptosis should enable the design of novel targeted therapies for these patients.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572013000100002
Editor:  Sociedade Brasileira de Genética
Relação:  10.1590/S1415-47572013005000003
Formato:  text/html
Fonte:  Genetics and Molecular Biology v.36 n.1 2013
Direitos:  info:eu-repo/semantics/openAccess
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