Putri Anastasia, Rinaldi Ikhwan, Louisa Melva, Koesnoe Soekamto
Department of Internal Medicine, Faculty of Medicine Universitas Indonesia, Jakarta, Indonesia.
Acta Med Indones. 2019 Oct;51(4):348-352.
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.
慢性髓系白血病（CML）是一种克隆性造血干细胞疾病，9号染色体（ch9）和22号染色体（ch22）发生相互易位，导致断裂簇区域-艾贝尔森鼠白血病（BCR-ABL）致癌基因融合。这种融合会激活酪氨酸激酶。甲磺酸伊马替尼是首个酪氨酸激酶抑制剂（TKI），它可以改变CML患者的预后。然而，存在对TKI的耐药性，基于转录组学研究，基因信号转导和转录激活因子（STAT）5A和 runt相关转录因子3（RUNX3）表达增加可导致对TKI产生耐药性。STAT5蛋白在正常髓细胞中由细胞因子激活，而在CML患者中即使没有细胞因子也被激活。STAT5指STAT5A和STAT5B，但它们在造血干细胞或CML细胞中可能具有不同作用。本综述总结了STAT5在CML患者酪氨酸激酶抑制剂耐药中的作用。
