Myeloproliferative neoplasms and the JAK/STAT signaling pathway: an overview
Rev. bras. hematol. hemoter
; Rev. bras. hematol. hemoter;37(5): 348-353, Sept.-Oct. 2015. tab, ilus
Article
em En
| LILACS
| ID: lil-764220
Biblioteca responsável:
BR408.1
Localização: BR408.1
ABSTRACT
ABSTRACTMyeloproliferative neoplasms are caused by a clonal proliferation of a hematopoietic progenitor. First described in 1951 as 'Myeloproliferative Diseases' and reevaluated by the World Health Organization classification system in 2011, myeloproliferative neoplasms include polycythemia vera, essential thrombocythemia and primary myelofibrosis in a subgroup called breakpoint cluster region-Abelson fusion oncogene-negative neoplasms. According to World Health Organization regarding diagnosis criteria for myeloproliferative neoplasms, the presence of the JAK2 V617F mutation is considered the most important criterion in the diagnosis of breakpoint cluster region-Abelson fusion oncogene-negative neoplasms and is thus used as a clonal marker. The V617F mutation in the Janus kinase 2(JAK2) gene produces an altered protein that constitutively activates the Janus kinase/signal transducers and activators of transcription pathway and other pathways downstream as a result of signal transducers and activators of transcription which are subsequently phosphorylated. This affects the expression of genes involved in the regulation of apoptosis and regulatory proteins and modifies the proliferation rate of hematopoietic stem cells.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Assunto principal:
Neoplasias Hematológicas
/
Fatores de Transcrição STAT
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Janus Quinase 2
Limite:
Female
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Humans
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Male
Idioma:
En
Revista:
Rev. bras. hematol. hemoter
Assunto da revista:
HEMATOLOGIA
Ano de publicação:
2015
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Brasil