Evidence map›Paper›PMID 12082526›Full record

ArticleOncogene2002

RNA polymerase III transcription can be derepressed by oncogenes or mutations that compromise p53 function in tumours and Li-Fraumeni syndrome.

Torsten Stein, Diane Crighton, John M Boyle, Jennifer M Varley, Robert J White

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Translation Control byCancers · 2018
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  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
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  13. Review
  14. Article
  15. The green tea component EGCG inhibits RNA polymerase III transcription.Biochemical and biophysical research communications · 2007
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Torsten SteinInstitute of Biomedical and Life Sciences, Division of Biochemistry and Molecular Biology, Davidson Building, University of Glasgow, Glasgow G12 8QQ, Scotland, UK.
Diane Crighton
John M Boyle
Jennifer M Varley
Robert J White
Cancer Research UK Manchester Institute · GBUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RNA polymerase (pol) III synthesizes essential small RNAs, including tRNA and 5S rRNA. Wild-type p53 can repress pol III transcription both in vitro and in vivo. Many tumours carry substitutions in p53 which have selective effects on its functions. We identify tumour-derived mutations that compromise the ability of p53 to regulate pol III transcription. Furthermore, substitution R175H, the most common mutation in cancers, converts p53 from a repressor to an activator of pol III. Oncoproteins neutralize p53 in some tumours; we show that human papillomavirus E6 and cellular hdm2 can both release pol III from repression by p53. These data suggest that the restraining influence of p53 on pol III will be lost in many tumours. In addition to these features of sporadic cancers, some individuals inherit mutant forms of p53 and consequently suffer from Li-Fraumeni syndrome, showing genetic predisposition to certain malignancies. We find that pol III transcriptional activity is often highly elevated in primary fibroblasts from Li-Fraumeni patients, especially if the germline p53 mutation is followed by loss of the remaining allele. Our data suggest that p53 status can have a profound effect upon pol III transcription and hence on the biosynthetic capacity of cells.

Indexed as

Genes, p53Nuclear ProteinsRepressor ProteinsAllelesAmino Acid SubstitutionBone NeoplasmsFibroblastsGene DeletionGene Expression Regulation, NeoplasticGerm-Line MutationHumansLi-Fraumeni SyndromeNeoplasm ProteinsOncogene Proteins, ViralOsteosarcomaPoint MutationE6 protein, Human papillomavirus type 16MDM2 protein, humanNeoplasm ProteinsNuclear ProteinsOncogene Proteins, ViralProto-Oncogene ProteinsProto-Oncogene Proteins c-mdm2Repressor ProteinsRNA Polymerase IIIRNA, Transfer, LeuTumor Suppressor Protein p53

Identifiers

PMID12082526
OpenAlexW2003438259

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.