Analysis of MicroRNA -155-5p Expression in Patients with Primary Myelofibrosis.
DOI:
https://doi.org/10.32007/jfacmedbaghdad.6642400Keywords:
Essential thrombocytosis, MicroRNA, Myeloproliferative neoplasms, Polycythemia Vera, Primary MyelofibrosisAbstract
Background: Primary myelofibrosis is a chronic myeloproliferative neoplasm characterized by abnormal megakaryocyte proliferation and fibrosis that destroys healthy bone marrow. This results in extramedullary hematopoiesis, variable blood cell deficiencies, hepatosplenomegaly, general symptoms, progression to leukemia, and a reduced lifespan. Myelofibrosis can occur as a de novo myeloproliferative neoplastic disorder or evolve from other myeloproliferative neoplasms, including Polycythemia Vera or Essential Thrombocytosis. MicroRNAs (miRNAs) are short, non-protein-coding RNA molecules, typically 18–24 nucleotides in length. Dysregulation of miRNAs may contribute to the disease phenotype.
Objective: To investigate the expression level of MicroRNA-155-5p in patients with Primary Myelofibrosis compared to healthy controls and its correlation with common clinic-pathological factors.
Methods: twenty-eight patients with Primary Myelofibrosis and twenty healthy subjects were examined as controls. Expression analysis of MicroRNA-155-5p was performed using reverse transcription-quantitative polymerase chain reaction (qRT-PCR) on plasma isolated from peripheral blood.
Results: MicroRNA-155-5p expression was significantly upregulated in patients with Primary Myelofibrosis (P = 0.0001). However, no significant correlations were found between MicroRNA-155-5p and age, sex, Janus kinase 2 mutation status, or hematological parameters, including hemoglobin, white blood cell count, and platelet count.
Conclusion: MicroRNA-155-5p expression is not influenced by age, sex, Janus kinase 2 mutation status, or hematological parameters. Aberrant expression of MicroRNA-155-5p may contribute to the pathogenesis of Primary Myelofibrosis, warranting further research to understand the disease mechanisms better.
Received: May. 2024
Revised: Aug. 2024
Accepted: Sept. 2024
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Copyright (c) 2024 Sarah I. Khaleel, Jaffar N. AlAlsaidissa
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