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.
Imatinib Mesylate/therapeutic use , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy , Protein Kinase Inhibitors/therapeutic use , STAT5 Transcription Factor/genetics , Tumor Suppressor Proteins/genetics , Drug Resistance, Neoplasm/genetics , Gene Expression Regulation, Neoplastic , Humans , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics , Protein-Tyrosine Kinases/antagonists & inhibitors , Pyrimidines
