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Int. J. Mol. Sci. 2016, 17(4), 570; doi:10.3390/ijms17040570

Downregulation of Plasma miR-215 in Chronic Myeloid Leukemia Patients with Successful Discontinuation of Imatinib

1
Department of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan
2
Department of Molecular Science, Tokyo Medical University, Tokyo 160-0023, Japan
3
Department of Molecular Oncology, Institute of Medical Science, Tokyo Medical University, Tokyo 160-0023, Japan
4
Department of Electrical Engineering, Kogakuin University, Tokyo 163-8677, Japan
*
Author to whom correspondence should be addressed.
Academic Editors: William Chi-shing Cho and Nalini Santanam
Received: 8 January 2016 / Revised: 14 March 2016 / Accepted: 8 April 2016 / Published: 15 April 2016
(This article belongs to the Special Issue MicroRNA in Various Disease States as Biomarkers)
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Abstract

Approximately 40% of chronic myeloid leukemia (CML) patients who discontinue imatinib (IM) therapy maintain undetectable minimal residual disease (UMRD) for more than one year (stopping IM (STOP-IM)). To determine a possible biomarker for STOP-IM CML, we examined plasma miRNA expression in CML patients who were able to discontinue IM. We first screened candidate miRNAs in unselected STOP-IM patients, who had sustained UMRD after discontinuing IM for more than six months, in comparison with healthy volunteers, by using a TaqMan low-density array for plasma or exosomes. Exosomal miR-215 and plasma miR-215 were downregulated in the STOP-IM group compared to the control, indicating that the biological relevance of the plasma miR-215 level is equivalent to that of the exosomal level. Next, we performed real-time quantitative RT-PCR in 20 STOP-IM patients, 32 patients with UMRD on continued IM therapy (IM group) and 28 healthy volunteers. The plasma miRNA-215 level was significantly downregulated in the STOP-IM group (p < 0.0001); we determined the cut-off level and divided the IM group patients into two groups according to whether the plasma miR-215 was downregulated or not. The IM group patients with a low plasma miR-215 level had a significantly higher total IM intake, compared to the patients with elevated miR-215 levels (p = 0.0229). Functional annotation of miR-215 target genes estimated by the Database for Annotation, Visualization and Integrated Discovery (DAVID) bioinformatic tools involved cell cycle, mitosis, DNA repair and cell cycle checkpoint. Our study suggests a possible role of miR-215 in successful IM discontinuation. View Full-Text
Keywords: plasma miR-215; chronic myeloid leukemia; imatinib; discontinuation plasma miR-215; chronic myeloid leukemia; imatinib; discontinuation
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Ohyashiki, K.; Umezu, T.; Katagiri, S.; Kobayashi, C.; Azuma, K.; Tauchi, T.; Okabe, S.; Fukuoka, Y.; Ohyashiki, J.H. Downregulation of Plasma miR-215 in Chronic Myeloid Leukemia Patients with Successful Discontinuation of Imatinib. Int. J. Mol. Sci. 2016, 17, 570.

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