Evidence map›Paper›PMID 33231252›Full record

ArticleJournal of radiation research2021

Strain difference in transgene-induced tumorigenesis and suppressive effect of ionizing radiation.

Bibek Dutta, Taichi Asami, Tohru Imatomi, Kento Igarashi, Kento Nagata, Tomomi Watanabe-Asaka, Takako Yasuda, Shoji Oda, Manfred Shartl, Hiroshi Mitani

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of radiation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 85% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 2 countries.

Bibek DuttaLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Taichi AsamiLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Tohru ImatomiLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Kento IgarashiLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Kento NagataLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Tomomi Watanabe-AsakaLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Takako YasudaLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Shoji OdaLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
Manfred ShartlUniversity of Wuerzburg, Physiological Chemistry, Biocenter, 97074 Wuerzburg, Germany and the Xiphophorus Genetic Stock Center, Department of Chemistry and Biochemistry, Texas State University, San Marcos, Texas, 78666, USA.
Hiroshi MitaniLaboratory of Genome Stability, Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 277-8562, Kashiwa, Japan.
The University of Tokyo · JPTexas State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic expression in medaka of the Xiphophorus oncogene xmrk, under a pigment cell specific mitf promoter, induces hyperpigmentation and pigment cell tumors. In this study, we crossed the Hd-rR and HNI inbred strains because complete genome information is readily available for molecular and genetic analysis. We prepared an Hd-rR (p53+/-, p53-/-) and Hd-rR HNI hybrid (p53+/-) fish-based xmrk model system to study the progression of pigment cells from hyperpigmentation to malignant tumors on different genetic backgrounds. In all strains examined, most of the initial hyperpigmentation occurred in the posterior region. On the Hd-rR background, mitf:xmrk-induced tumorigenesis was less frequent in p53+/- fish than in p53-/- fish. The incidence of hyperpigmentation was more frequent in Hd-rR/HNI hybrids than in Hd-rR homozygotes; however, the frequency of malignant tumors was low, which suggested the presence of a tumor suppressor in HNI genetic background fish. The effects on tumorigenesis in xmrk-transgenic immature medaka of a single 1.3 Gy irradiation was assessed by quantifying tumor progression over 4 consecutive months. The results demonstrate that irradiation has a different level of suppressive effect on the frequency of hyperpigmentation in purebred Hd-rR compared with hybrids.

Indexed as

Radiation, IonizingTransgenesAnimalsAnimals, Genetically ModifiedCarcinogenesisCyprinodontiformesDose-Response Relationship, RadiationFish ProteinsGamma RaysHybridization, GeneticHyperpigmentationReceptor Protein-Tyrosine KinasesTumor Suppressor Protein p53Fish ProteinsReceptor Protein-Tyrosine KinasesTumor Suppressor Protein p53Xmrk protein, Xiphophorusirradiationmedakamitfp53tumorxmrk

Identifiers

PMID33231252
PMCPMC7779347
OpenAlexW3108099180

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.