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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

Department of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan
Department of Molecular Science, Tokyo Medical University, Tokyo 160-0023, Japan
Department of Molecular Oncology, Institute of Medical Science, Tokyo Medical University, Tokyo 160-0023, Japan
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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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

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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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