Evidence map›Paper›PMID 29071477›Full record

ArticleInternational journal of hematology2018

Enforced expression of MIR142, a target of chromosome translocation in human B-cell tumors, results in B-cell depletion.

Kodai Kuriyama, Yutaka Enomoto, Ritsuro Suzuki, Jyuri Watanuki, Hiroki Hosoi, Yusuke Yamashita, Shogo Murata, Toshiki Mushino, Shinobu Tamura, Nobuyoshi Hanaoka and 6 more

Abstract read
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In one paragraph

Article in International journal of hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Review
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

16 authors at 5 institutions in 3 countries.

Kodai KuriyamaHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Yutaka EnomotoDivision of Cellular Therapy and Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ritsuro SuzukiHematology and Oncology, Shimane Medical University, Shimane, Japan.
Jyuri WatanukiHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Hiroki HosoiHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Yusuke YamashitaHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Shogo MurataHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Toshiki MushinoHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Shinobu TamuraHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Nobuyoshi HanaokaHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Martin DyerDepartment of Cancer Studies and Molecular Medicine, Leicester Medical School, University of Leicester, Leicester, UK.
Reiner SiebertInstitute of Human Genetics, Christian Albrechts University Kiel, Kiel, Germany.
Hiroshi KiyonariAnimal Resource Development Unit, RIKEN Center for Life Science Technologies, Kobe, Japan.
Hideki NakakumaHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan.
Toshio KitamuraDivision of Cellular Therapy and Division of Stem Cell Signaling, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Takashi SonokiHematology/Oncology, Wakayama Medical University, 811-1 Kimi-idera, Wakayama, 641-8510, Japan. sonoki@wakayama-med.ac.jp.
Wakayama Medical University · JPThe University of Tokyo · JPKiel University · DEShimane University · JPUniversity of Leicester · GB

Funding

Medical Research Council MC_U132670597The Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan no. 25461433Wakayama Medical University (JP) 2014Wakayama Medical University (JP) a Research Grant on Priority Areas
6 · The paper itself

Abstract

MicroRNA142 (MIR142) is a target of chromosome translocations and mutations in human B-cell lymphomas. We analyzed an aggressive B-cell lymphoma carrying t(8;17)(q24;q22) and t(6;14)(p21;q32), and sought to explore the role(s) of MIR142 in lymphomagenesis. t(8;17)(q24;q22) involved MYC on 8q24 and pri-MIR142 on 17q22. MYC was activated by a promoter substitution by t(8;17)(q24;q22). t(8;17)(q24;q22) was an additional event after t(6;14) (p21;q32), which caused the over-expression of CCND3. Southern blot analyses revealed that the MIR142 locus was deleted from the affected allele, whereas Northern analyses showed over-expression of MIR142 in tumor cells. Although previous studies reported an over-expression of mutations in MIR142 in B-cell lymphomas, limited information is available on the functions of MIR142 in lymphomagenesis. Therefore, we generated bone marrow transplantation (BMT) and transgenic (Eμ/mir142) mice, which showed enforced expression in hematopoietic progenitor cells and B cells, respectively. BMT mice showed decreased numbers of all lineage-positive cells, particularly B cells, in peripheral blood. Eμ/mir142 mice showed decreased numbers of IgM-positive splenocytes, and exhibited altered B-cell phenotypic changes induced by lipopolysaccharide. Our results suggest that over-expression of MIR142 alters B-cell differentiation, implying multi-step lymphomagenesis together with MYC activation and CCND3 over-expression.

Indexed as

AnimalsB-LymphocytesCell DifferentiationCell Line, TumorChromosomes, Human, Pair 14Chromosomes, Human, Pair 8Gene ExpressionHumansLymphoma, B-CellMice, TransgenicMicroRNAsTranslocation, GeneticMicroRNAsMIRN142 microRNA, humanB-lymphomaCCND3Chromosome translocationMicroRNA142MYC

Identifiers

PMID29071477
OpenAlexW2766968433

What OpenQuestion holds

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Registered trials

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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.