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The Role of Micrornas in Myeloproliferative Neoplasia



Alizadeh S1 ; Azizi SG1 ; Soleimani M2 ; Farshi Y1 ; Khatib ZK2
Authors
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Authors Affiliations
  1. 1. Hematology Department, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Hematology Department, School of Medicine, Tarbiat Modares University, Tehran, Iran

Source: International Journal of Hematology-Oncology and Stem Cell Research Published:2016

Abstract

MiRs are 17-25 nucleotide non-coding RNAs. These RNAs target approximately 80% of protein coding mRNAs. MiRs control gene expression and altered expression of them affects the development of cancer. MiRs can function as tumor suppressor via down-regulation of proto-oncogenes and may function as oncogenes by suppressing tumor suppressors. Myeloproliferative neoplasias (formerly known as chronic myeloproliferative disorders) form a class of hematologic malignancies demonstrating the expansion of stem cells in one or more hematopoietic cell lines. CML results from an acquired translocation known as BCR-ABL (Philadelphia chromosome). JAK2V617F mutation is present in over 95% of PV, 55% of ET and 65% of PMF cases. Aberrant expression of miR is associated with myeloproliferative neoplasias, pathogenesis, disease progress and response to treatment. MiRs can also be potential therapeutic targets. CML is mainly treated by tyrosine kinase inhibitors such as Imatinib. In addition, altered function of miRs may be used as a prognostic factor in treatment. Resistance to Imatinib is currently a major clinical problem. The role of a number of miRs has been demonstrated in this resistance. Changing expression pattern of miRs can be effective in response to treatment and inhibition of drug resistance. In this paper, we set out to evaluate the effect of miRs in pathogenesis and treatment of MPN. © 2016, Tehran University of Medical Sciences (TUMS). All rights reserved.
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