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Inhibitors of JAK2/STAT Signaling Pathway and Hematologic Malignancies-Review / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 1275-1279, 2016.
Artigo em Chinês | WPRIM | ID: wpr-246776
ABSTRACT
Jauns kinase (JAK)/transducer and activator of transcription(STAT) pathway is a classical approach to study the rapid changes of the gene expression in specific target cells by a variety of extracellular signals. The JAK and STAT transfer cytokine receptor signaling plays a unique role in multiple cellular and molecular biological changes.The abnormal signal of JAK/STAT pathway will lead to the hematopoietic abnormalities.Studies had shown that the abnormal activation of JAK2/STAT signaling pathway are in many kinds of malignant hematological diseases, such as in acute lymphoblastic/myeloid leukemia, chronic myeloid leukemia, lymphoma, myelodysplastic syndromes, myeloprofilerative neoplasm, especially in the patients of myeloproliferative neoplasm(MPN) with JAK gene mutation(JAK2V617F), this mutation has an important value for MPN diagnosis. At present, the effect of the specific inhibitors of JAK2 has showed good perspective, which had been applied to clinic treatment and achieved remarkable curative effect. In this review, the JAK2/STAT signaling transduction, the JAK2 signal and hematologic malignancies, the kagulation of signaling pathway and the inhibitors of JAK2/STAT signaling pathway are summarized.
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Transdução de Sinais / Neoplasias Hematológicas / Fatores de Transcrição STAT / Janus Quinase 2 / Mutação Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Transdução de Sinais / Neoplasias Hematológicas / Fatores de Transcrição STAT / Janus Quinase 2 / Mutação Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo