Abstract
Chronic myeloid leukemia (CML) is a clonal neoplasm originating from hematopoietic stem cells which is characterized by t(9;22)(q34;q11.2) fusion gene leading to forming an oncoprotein. miR-411 and SPRY4 may influence CML leukemogenesis by regulating proliferation, differentiation, and various signaling pathways induced by the oncoprotein. In this cross-sectional study, a total of 90 blood samples were collected from individuals diagnosed with CML, covering three distinct clinical phases: 38 samples at the diagnosis, 38 samples one year after treatment with imatinib, and 14 samples during the blastic phase. The expression levels of miR-411 and SPRY4 genes were measured using real-time PCR. Statistical analysis was conducted using nonparametric tests. Using the Mann-Whitney U test, miR-411 expression was significantly upregulated post-treatment compared to the time of diagnosis (fold change: 15.6; P < 0.0001), and downregulated in the blastic phase compared to the post-treatment phase (fold change: 1.84; P = 0.01). In contrast, SPRY4 expression was significantly downregulated post-treatment compared to the time of diagnosis (fold change: 4.5; P = 0.03), and upregulated in the blastic phase compared to the post-treatment phase (fold change: 7.8; P = 0.001). This study suggests that SPRY4 and miR-411 may exert phase-specific roles in CML progression probably with reverse pattern, although further studies are needed to clarify the role of these two genes in hematological malignancies such as CML.