Evidence map›Paper›PMID 10391680›Full record

ArticleOncogene1999

Cooperative activity between HER oncogenes and the tumor suppressor IRF-1 results in apoptosis.

S Kirchhoff, H Hauser

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 44 citations in OpenAlex.

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  7. Elevated level of SUMOylated IRF-1 in tumor cells interferes with IRF-1-mediated apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2007
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  16. Interplay between DNA repair and inflammation, and the link to cancer.Critical reviews in biochemistry and molecular biology
    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

2 authors at 1 institution in 1 country.

S KirchhoffDepartment of Gene Regulation and Differentiation, GBF-National Research Center for Biotechnology, Braunschweig, Germany.
H Hauser
Helmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor transcription factor IRF-1 inhibits cell growth. In this report we show that IRF-1 also induces apoptosis of highly transformed and tumorigenic cell lines. This activity of IRF-1 is demonstrated with cell lines expressing HER oncogenes and an activatable IRF-1 fusion protein. Growth of cell lines expressing inactive HER1 is inhibited on IRF-1 activation. In contrast, the same cells are killed by apoptosis when HER1 and IRF-1 are activated simultaneously. We identified promoters stimulated synergistically by IRF-1 and by activated HER1. To determine the signals causing transcriptional synergism and/or apoptosis we tried to modulate these effects by various dominant negative acting proteins. Dominant negative STAT5alpha abolished both induction of apoptosis and transcriptional synergy of IRF-1 and HER. Thus, these results provide new insights into the mechanism of oncogene-dependent apoptosis induced by the activation of a tumor suppressor.

Indexed as

Genes, Tumor SuppressorMilk ProteinsOncogenes3T3 CellsAdenovirus E1A ProteinsAdenovirus E1B ProteinsAnimalsCell Line, TransformedCell Transformation, ViralDNA-Binding ProteinsEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsEstradiolGene Expression Regulation, NeoplasticHumansAdenovirus E1A ProteinsAdenovirus E1B ProteinsDNA-Binding ProteinsEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsEstradiolInterferon Regulatory Factor-1InterferonsIRF1 protein, humanIrf1 protein, mouseMilk ProteinsPhosphoproteinsras ProteinsRecombinant Fusion ProteinsSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID10391680
OpenAlexW2037627988

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.