Abstract
Chronic myeloid leukemia (CML), is a myeloproliferative disease characterized by unregulated growth of blood forming cells in bone marrow and blood. The t(9;22)(q34;q11.2) translocation, which results in the formation of a hyperactive tyrosine kinase (BCR-ABL), is a hallmark of this disorder. Tyrosine kinase inhibitors such as imatinib has shown a great promise in reduction of CML cells. However, development of resistance to tyrosine kinase inhibitors has raised a great clinical concern about their future applications. Recently, non-coding RNAs, have shown to play significant regulatory roles in development of chemoresistance in CML cells. Discovering the underlying mechanisms of these non-coding RNAs might provide new opportunities for treating chemo-resistant forms of CML. These non-coding RNAs could be considered valuable therapeutic targets if they are found to play a role in the development of chemoresistance in CML cells. We mentioned the identified non-coding RNAs in development of chemoresistance in CML cells.