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<p>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; <i>P</i> &lt; 0.0001), and downregulated in the blastic phase compared to the post-treatment phase (fold change: 1.84; <i>P</i> = 0.01). In contrast, SPRY4 expression was significantly downregulated post-treatment compared to the time of diagnosis (fold change: 4.5; <i>P</i> = 0.03), and upregulated in the blastic phase compared to the post-treatment phase (fold change: 7.8; <i>P</i> = 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.</p>

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Expression profiles of miR-411 and SPRY4 as indicators of disease progression and treatment in chronic myelogenous leukemia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月20日

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  • Ashkan Shabannezhad,
  • Nasrin Alizadghandforoush,
  • Majid Safa,
  • Shahrbano Rostami,
  • Bahram Chahardouli,
  • Ali Amini

摘要

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.