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Effect of methylation inhibitor in the treatment of leukemia / 中国实验血液学杂志
Article em Zh | WPRIM | ID: wpr-332741
Biblioteca responsável: WPRO
ABSTRACT
More and more studies have found that the occurrence of tumors are directly related to the abnormal expression of oncogene and antioncogene. If the antioncogene is mutated or absent, the function of cells will be weakened and inactivated, the cells will be duplicated repeatedly out of control, then will induce occurrence and metastasis of tumor. For example, SHP-1 tyrosine phosphatase, as an antioncogene, is a key negative regulator in signaling transduction of haematopoietic cells. The decrease and silence of SHP-1 play an important role in tumorigenesis. If the oncogene in leukemia patients lost the effect of negative regulation of antioncogene, the oncogene would be expressed abnormally high, such as the oncogene c-kit (an important member of the class III in the tyrosine kinase receptor family) in many kinds of leukemia cells expresses actively. Studies have shown that the high methylation of promoter region would induce the inactivation of tumor suppressor and active expression of oncogene, therefore, the restoring normal methylation of promoter region will contribute to restoration of normal gene expression, thus achieving the purpose of gene therapy for leukemia. In this article, the methylation, methylation abnormality and leukemia, methylation suppressors and therapy of leukemia are briefly reviewed.
Assuntos
Texto completo: 1 Índice: WPRIM Assunto principal: Leucemia / Metilação de DNA / Tratamento Farmacológico / Proteína Tirosina Fosfatase não Receptora Tipo 6 / Metabolismo Limite: Humans Idioma: Zh Revista: Journal of Experimental Hematology Ano de publicação: 2013 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Leucemia / Metilação de DNA / Tratamento Farmacológico / Proteína Tirosina Fosfatase não Receptora Tipo 6 / Metabolismo Limite: Humans Idioma: Zh Revista: Journal of Experimental Hematology Ano de publicação: 2013 Tipo de documento: Article