The Role of STAT5 in Tyrosine Kinase Inhibitor (IMATINIB) Resistance in CML Patients.
Acta Med Indones
; 51(4): 348-352, 2019 Oct.
Article
em En
| MEDLINE
| ID: mdl-32041920
Chronic myeloid leukemia (CML) is a clonal haemopoietic stem cell disorders with reciprocal translocation in chromosome 9 (ch9) and 22 (ch22) which cause the fusion of Break cluster region-Abelson murine leukemia (BCR-ABL) oncogene. This fusion will activate tyrosine kinase. Imatinib mesylate is the first tyrosine kinase inhibitor (TKI), which could change the prognosis of CML patients. However, there is a resistance to TKI's, and based on transcriptomic study, increase expression of gen signal transducer and activator of transcription (STAT) 5A and runt-related transcription factor 3 (RUNX3) can cause resistance to TKI's. The STAT5 protein, which in normal myeloid cells being activated by cytokine, in CML patients was activated even without cytokines. STAT5 refer to STAT5A and STAT5B, however they have might have different role in hematopoietic stem cells or in CML cells. This review summarizes the role of STAT5 in tyrosine kinase inhibitor resistance in CML patients.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Leucemia Mielogênica Crônica BCR-ABL Positiva
/
Proteínas Supressoras de Tumor
/
Inibidores de Proteínas Quinases
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Fator de Transcrição STAT5
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Mesilato de Imatinib
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Acta Med Indones
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Indonésia