Evidence map›Paper›PMID 27092489›Full record

ArticleInternational journal of molecular sciences2016

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

Kazuma Ohyashiki, Tomohiro Umezu, Seiichiro Katagiri, Chiaki Kobayashi, Kenko Azuma, Tetsuzo Tauchi, Seiichi Okabe, Yutaka Fukuoka, Junko H Ohyashiki

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  4. The theragnostic advances of exosomes in managing leukaemia.Journal of cellular and molecular medicine · 2024
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  18. Focus on exosomes: novel pathogenic components of leukemia.American journal of cancer research · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Kazuma OhyashikiDepartment of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan. ohyashik@rr.iij4u.or.jp.
Tomohiro UmezuDepartment of Molecular Science, Tokyo Medical University, Tokyo 160-0023, Japan. t_umezu@tokyo-med.ac.jp.
Seiichiro KatagiriDepartment of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan. patchsei@yahoo.co.jp.
Chiaki KobayashiDepartment of Molecular Science, Tokyo Medical University, Tokyo 160-0023, Japan. chiaki-k@tokyo-med.ac.jp.
Kenko AzumaDepartment of Molecular Oncology, Institute of Medical Science, Tokyo Medical University, Tokyo 160-0023, Japan. k_azuma@tokyo-med.ac.jp.
Tetsuzo TauchiDepartment of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan. tauchi@tokyo-med.ac.jp.
Seiichi OkabeDepartment of Hematology, Tokyo Medical University, Tokyo 160-0023, Japan. okabe@tokyo-med.ac.jp.
Yutaka FukuokaDepartment of Electrical Engineering, Kogakuin University, Tokyo 163-8677, Japan. fukuoka@cc.kogakuin.ac.jp.
Junko H OhyashikiDepartment of Molecular Oncology, Institute of Medical Science, Tokyo Medical University, Tokyo 160-0023, Japan. junko@hh.iij4u.or.jp.
Tokyo Medical University · JPKogakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Antineoplastic AgentsDown-RegulationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMicroRNAsAntineoplastic AgentsImatinib MesylateMicroRNAsMIRN215 microRNA, humanchronic myeloid leukemiadiscontinuationimatinibplasma miR-215

Identifiers

PMID27092489
PMCPMC4849026
OpenAlexW2339515029

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.