Evidence map›Paper›PMID 26676972›Full record

ArticleInternational journal of oncology2016

Identification of miR-15b as a transformation-related factor in mantle cell lymphoma.

Fumiko Arakawa, Yoshizo Kimura, Noriaki Yoshida, Hiroaki Miyoshi, Atushi Doi, Kaori Yasuda, Kazutaka Nakajima, Junichi Kiyasu, Daisuke Niino, Yasuo Sugita and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

14 authors.

Fumiko ArakawaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Yoshizo KimuraDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Noriaki YoshidaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Hiroaki MiyoshiDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Atushi DoiCell Innovator Inc., Venture Business Laboratory of Kyushu University, Fukuoka, Japan.
Kaori YasudaCell Innovator Inc., Venture Business Laboratory of Kyushu University, Fukuoka, Japan.
Kazutaka NakajimaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Junichi KiyasuDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Daisuke NiinoDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Yasuo SugitaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Kosuke TashiroLaboratory of Molecular Gene Technology and Molecular Biosciences, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, Fukuoka, Japan.
Satoru KuharaLaboratory of Molecular Gene Technology and Molecular Biosciences, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, Fukuoka, Japan.
Masao SetoDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.
Koichi OhshimaDepartment of Pathology, School of Medicine, Kurume University, Kurume, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mantle cell lymphoma (MCL) is an aggressive B cell lymphoma with a poor prognosis. It is characterized by the t(11;14)(q13;q32) translocation, resulting in over-expression of CCND1. Morphologically, MCL is categorised into two types: classical MCL (cMCL) and aggressive MCL (aMCL), with a proportion of cMCL progressing to develop into aMCL. miRNAs are currently considered to be important regulators for cell behavior and are deregulated in many malignancies. Although several genetic alterations have been implicated in the transformation of cMCL to aMCL, the involvement of miRNAs in transformation is not known. In an effort to identify the miRNAs related to the transformation of MCL, miRNA microarray analyses were used for cMCL and aMCL cases. These analyses demonstrated significant differences in the expression of seven microRNAs based on a t-test (p-value <0.05); miR-15b was greatly upregulated in aMCL. Locked nucleic acid in situ hybridization showed increased staining of miR-15b in formalin-fixed paraffin-embedded sections of aMCL. These results correlated well with the microRNA microarray analysis. Although the molecular functions of miR-15b are largely unknown, it has been found to be associated with the cell cycle and apoptosis. However, the physiological significance of increased miR-15b in MCL is still unknown. Our present findings suggest that the upregulated expression of miR-15b is likely to play an important role in the trans-formation of cMCL to aMCL.

Indexed as

AgedAged, 80 and overApoptosisBiomarkers, TumorCell CycleCyclin D1FemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLymphoma, B-CellLymphoma, Mantle-CellMaleMicroarray AnalysisMicroRNAsMiddle AgedBiomarkers, TumorCCND1 protein, humanCyclin D1MicroRNAsMIRN15 microRNA, human

Identifiers

PMID26676972
PMCPMC4725451

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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.