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ORIGINAL ARTICLE
Year : 2019  |  Volume : 32  |  Issue : 3  |  Page : 1004-1008

Decreased expression of microRNA-451 is associated with imatinib mesylate resistance in patients with chronic myeloid leukemia


1 Department of Clinical Pathology, Faculty of Medicine, Menoufia University, National Liver Institute, Menoufia, Egypt
2 Department of Clinical Pathology, National Liver Institute, Menoufia University, Menoufia, Egypt
3 Department of Medical Oncology, National Cancer Institute, Cairo University, Cairo, Egypt
4 Department of Clinical Oncology, Faculty of Medicine, Menoufia University, National Liver Institute, Menoufia, Egypt

Correspondence Address:
Sally S Mandour Esawy
Department of Clinical Pathology, National Liver Institute, Menoufia University, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_130_19

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Objectives To measure the expression levels of microRNA-451 (miR-451) in patients with chronic myeloid leukemia (CML) and to correlate miR-451 expression levels with response to imatinib mesylate (IM)-based therapeutic protocol. Background miRNAs are regulatory RNAs that have been classified as crucial players of cancer initiation and progression. Recent studies have illustrated an association between certain hematological malignancies and dysregulated miRNAs expressions; other studies have focused on the utilization of miRNAs as molecular biomarkers of cancer detection, outcome, and response to therapy. Patients and methods Real-time quantitative PCR technique was used to estimate the plasma miR-451 expression levels of 10 newly diagnosed patients and 30 patients with CML who received first-line therapy with imatinib. European Leukemia Net-recommended response criteria were used to classify patients according to their response to imatinib treatment. Results Our results revealed up-regulation of miR-451 expression levels in imatinib treated as compared with newly diagnosed patients with CML (P = 0.003). MiR-451 expression was significantly upregulated in IM-responder when compared with the IM-resistant group (P < 0.001). Moreover, we demonstrated that miR-451 was significantly down-regulated in IM-resistant in comparison with the healthy control group (P < 0.001), whereas no significant difference was detected between IM-responder group and healthy controls (P = 0.620). Conclusion miR-451 can be used as a promising biomarker in patients with CML for prediction of imatinib treatment response and may be employed as a novel therapeutic tool.


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