Evidence map›Paper›PMID 25728674›Full record

ReviewOncogene2015

p53, a translational regulator: contribution to its tumour-suppressor activity.

V Marcel, F Catez, J-J Diaz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. 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
6.2field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 87 citations in OpenAlex.

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  12. ABiomedicines · 2022
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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

3 authors at 2 institutions in 1 country.

V MarcelCancer Cell Plasticity Department, Centre de Recherche en Cancérologie de Lyon, UMR INSERM 1052 CNRS 5286, Centre Léon Bérard, Lyon, France.
F CatezCancer Cell Plasticity Department, Centre de Recherche en Cancérologie de Lyon, UMR INSERM 1052 CNRS 5286, Centre Léon Bérard, Lyon, France.
J-J DiazCancer Cell Plasticity Department, Centre de Recherche en Cancérologie de Lyon, UMR INSERM 1052 CNRS 5286, Centre Léon Bérard, Lyon, France.
Centre Léon Bérard · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A growing body of evidences indicate that deregulation of translation contributes to tumourigenesis. In tumours, alterations of translational control of specific mRNAs encoding oncogenes or tumour suppressors have been extensively reported. Moreover, restricting the rate of protein synthesis has been shown to delays tumourigenesis in C-Myc overexpressing or PTEN deleted mice models. Finally, the specific inhibition of RNA polymerase I (RNA pol I) has been shown to kill cancer cells without affecting normal cells. It thus emerges that a tight coordination between the rate of global protein synthesis and a defined translational program is required to prevent tumour development. In this review, we expose the evidences supporting that p53 acts as a translational regulator. In addition, this review discusses the notion that the ability to maintain both a selective translational program and a low level of protein synthesis could directly contribute to the p53 tumour-suppressor activity.

Indexed as

AnimalsCarcinogenesisGenes, Tumor SuppressorHumansNeoplasmsProtein BiosynthesisRNA, MessengerTumor Suppressor Protein p53RNA, MessengerTumor Suppressor Protein p53

Identifiers

PMID25728674
OpenAlexW2043215375

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.