Evidence map›Paper›PMID 24978700›Full record

ArticlePloS one2014

Allelic imbalance in the miR-31 host gene locus in lung cancer--its potential role in carcinogenesis.

Koji Okudela, Yoko Tateishi, Shigeaki Umeda, Hideaki Mitsui, Takeshisa Suzuki, Yuichi Saito, Tetsukan Woo, Michihiko Tajiri, Munetaka Masuda, Yohei Miyagi and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Function and regulation of microRNA-31 in development and disease.Molecular reproduction and development · 2016
    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

11 authors at 3 institutions in 1 country.

Koji OkudelaDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yoko TateishiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Shigeaki UmedaDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hideaki MitsuiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Takeshisa SuzukiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yuichi SaitoDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Tetsukan WooDepartment of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Michihiko TajiriDivision of General Thoracic Surgery, Kanagawa Cardiovascular and Respiratory Disease Center Hospital, Yokohama, Japan.
Munetaka MasudaDepartment of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yohei MiyagiClinical Research Institute, Kanagawa Prefectural Cancer Center Hospital, Yokohama, Japan.
Kenichi OhashiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yokohama City University · JPKanagawa Cardiovascular and Respiratory Center · JPKanagawa Prefectural Hospital Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small non-protein coding RNA, microRNA (miR), which regulate messenger RNA levels, have recently been identified, and may play important roles in the pathogenesis of various diseases. The present study focused on miR-31 and investigated its potential involvement in lung carcinogenesis. The expression of miR-31 was altered in lung cancer cells through either the amplification or loss of the host gene locus. The strong expression of miR-31 in large cell carcinomas was attributed to the gene amplification. Meanwhile, the loss of miR-31 expression was more frequently observed in aggressive adenocarcinomas. Thus, miR-31 may play a pleiotropic role in the development of lung cancers among different histological types. To the best of our knowledge, this is the first study to show the potential causative mechanism of the altered expression of miR-31 and suggest its potentially diverse significance in the different histological types of lung cancers.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAllelic ImbalanceCarcinogenesisCarcinoma, Large CellCarcinoma, Small CellCarcinoma, Squamous CellCell Line, TumorGene DosageGenetic LociGenetic PleiotropyHumansLung NeoplasmsMicroRNAsMicroRNAsMIRN31 microRNA, human

Identifiers

PMID24978700
PMCPMC4076198
OpenAlexW1983824430

What OpenQuestion holds

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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.