Evidence map›Paper›PMID 10346812›Full record

ArticleGenes & development1999

Loss of transcription factor IRF-1 affects tumor susceptibility in mice carrying the Ha-ras transgene or nullizygosity for p53.

H Nozawa, E Oda, K Nakao, M Ishihara, S Ueda, T Yokochi, K Ogasawara, Y Nakatsuru, S Shimizu, Y Ohira and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed, 123 citations in OpenAlex.

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  11. ZBED2 is an antagonist of interferon regulatory factor 1 and modifies cell identity in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

17 authors at 4 institutions in 1 country.

H NozawaDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
E Oda
K Nakao
M Ishihara
S Ueda
T Yokochi
K Ogasawara
Y Nakatsuru
S Shimizu
Y Ohira
K Hioki
S Aizawa
T Ishikawa
M Katsuki
T Muto
T Taniguchi
N Tanaka
Tokyo University of Science · JPCentral Institute for Experimental Animals · JPThe University of Tokyo · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor IRF-1 has been implicated in tumor suppression: IRF-1 suppresses cell transformation and mediates apoptosis in vitro. Here we show that the loss of IRF-1 alleles per se has no effect on spontaneous tumor development in the mouse but dramatically exacerbates previous tumor predispositions caused by the c-Ha-ras transgene or by nullizygosity for p53. Grossly altered tumor spectrum, as compared to p53-null mice, was also observed in mice lacking both IRF-1 and p53, and cells from these mice show significantly higher mutation rate. Our results suggest that IRF-1 is a new member of the tumor susceptibility genes.

Indexed as

Genetic Predisposition to DiseaseAnimalsCells, CulturedCisplatinDNA-Binding ProteinsFemaleGenes, p53GenotypeInterferon Regulatory Factor-1MaleMethylnitronitrosoguanidineMiceMice, TransgenicMutagenesisMutagensNeoplasms, ExperimentalCisplatinDNA-Binding ProteinsInterferon Regulatory Factor-1Irf1 protein, mouseMethylnitronitrosoguanidineMutagensPhosphoproteins

Identifiers

PMID10346812
PMCPMC316726
OpenAlexW2139154967

What OpenQuestion holds

Textmetadata
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.