Evidence map›Paper›PMID 27338035›Full record

ArticleCancer research and treatment2017

Gastric Carcinogenesis in the miR-222/221 Transgenic Mouse Model.

Boram Choi, Jieun Yu, Tae-Su Han, Young-Kook Kim, Keun Hur, Byeong-Cheol Kang, Woo-Ho Kim, Dae-Yong Kim, Hyuk-Joon Lee, V Narry Kim and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Cancer research and treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

11 authors at 5 institutions in 2 countries.

Boram ChoiCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Jieun YuCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Tae-Su HanDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Young-Kook KimCenter for RNA Research, Institute for Basic Science, Korea School of Biological Sciences, Seoul National University, Seoul, Korea.
Keun HurDepartment of Biochemistry and Cell Biology, Cell and Matrix Research Institute, Kyungpook National University School of Medicine, Daegu, Korea.
Byeong-Cheol KangDepartment of Experimental Animal Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea.
Woo-Ho KimCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Dae-Yong KimCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Hyuk-Joon LeeCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
V Narry KimCenter for RNA Research, Institute for Basic Science, Korea School of Biological Sciences, Seoul National University, Seoul, Korea.
Han-Kwang YangCancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University · KRInstitute for Basic Science · KRKanazawa University · JPKyungpook National University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMicroRNAs (miRNAs) regulate various cellular functions, including development, cell proliferation, apoptosis, and tumorigenesis. Different signatures associated with various tissue types, diagnosis, progression, prognosis, staging, and treatment response have been identified by miRNA expression profiling of human tumors. miRNAs function as oncogenes or as tumor suppressors. The relationship between gastric cancer and miRNA garnered attention due to the high incidence of gastric cancer in Asian countries. miR-222/221 expression increases in gastric tumor tissues. The oncogenic effect of miR-222/221 was previously determined in functional studies and xenograft models. In this study, transgenic mice over-expressing miR-222/221 were generated to confirm the effect of miR-222/221 on gastric carcinogenesis. MATERIALS AND

methodsAt 6 weeks of age, 65 transgenic mice and 53 wild-type mice were given drinking water containing

resultsHyperplasia was observed in 3.77% of the wild-type mice and in 18.46% of the transgenic mice (p=0.020). Adenoma was observed in 20.75% of the wild-type mice and 26.15% of the transgenic mice (p=0.522). Carcinoma was observed in 32.08% of the wild-type mice and 41.54% of the transgenic mice (p=0.341). The frequency of hyperplasia, adenoma, and carcinoma was higher in transgenic mice, but the difference was statistically significant only in hyperplasia.

conclusionThese results suggest that hyperplasia, a gastric pre-cancerous lesion, is associated with miR-222/221 expression but miR-222/221 expression does not affect tumorigenesis itself.

Indexed as

Genetic Predisposition to DiseaseAnimalsBiomarkers, TumorCarcinogensCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalGenetic Association StudiesHumansImmunohistochemistryMiceMice, TransgenicMicroRNAsPhenotypeStomach NeoplasmsBiomarkers, TumorCarcinogensMicroRNAsMIRN221 microRNA, mouseMIRN222 microRNA, mouseGastric carcinogenesismicroRNAsMNU (N-nitroso-N-methylurea)Stomach neoplasmsTransgenic mouse

Identifiers

PMID27338035
PMCPMC5266385
OpenAlexW2469603272

What OpenQuestion holds

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LicenceCC BY-NC
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.