Evidence map›Paper›PMID 17347683›Full record

ArticleThe Journal of clinical investigation2007

A p53-derived apoptotic peptide derepresses p73 to cause tumor regression in vivo.

Helen S Bell, Christine Dufes, Jim O'Prey, Diane Crighton, Daniele Bergamaschi, Xin Lu, Andreas G Schätzlein, Karen H Vousden, Kevin M Ryan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Loss of autophagy causes a synthetic lethal deficiency in DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Graft-versus-host disease-related cytokine-driven apoptosis depends on p73 in cytokeratin 15-positive target cells.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2012
    Article
  17. Article
  18. Article
  19. p73 as a pharmaceutical target for cancer therapy.Current pharmaceutical design · 2011
    Review
  20. Pharmacological activation of p53 in cancer cells.Current pharmaceutical design · 2011
    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

9 authors at 5 institutions in 1 country.

Helen S BellTumour Cell Death Laboratory, Beatson Institute for Cancer Research, Glasgow, United Kingdom.
Christine Dufes
Jim O'Prey
Diane Crighton
Daniele Bergamaschi
Xin Lu
Andreas G Schätzlein
Karen H Vousden
Kevin M Ryan
Cancer Research UK Scotland Institute · GBLudwig Cancer Research · GBUniversity College London · GBUniversity of Glasgow · GBUniversity of Strathclyde · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53 is a potent inducer of tumor cell death, and strategies exist to exploit p53 for therapeutic gain. However, because about half of human cancers contain mutant p53, application of these strategies is restricted. p53 family members, in particular p73, are in many ways functional paralogs of p53, but are rarely mutated in cancer. Methods for specific activation of p73, however, remain to be elucidated. We describe here a minimal p53-derived apoptotic peptide that induced death in multiple cell types regardless of p53 status. While unable to activate gene expression directly, this peptide retained the capacity to bind iASPP - a common negative regulator of p53 family members. Concordantly, in p53-null cells, this peptide derepressed p73, causing p73-mediated gene activation and death. Moreover, systemic nanoparticle delivery of a transgene expressing this peptide caused tumor regression in vivo via p73. This study therefore heralds what we believe to be the first strategy to directly and selectively activate p73 therapeutically and may lead to the development of broadly applicable agents for the treatment of malignant disease.

Indexed as

Gene Expression Regulation, NeoplasticGenes, p53AnimalsApoptosisCell DeathCell Line, TumorDNA-Binding ProteinsHumansMiceMice, KnockoutMice, TransgenicNeoplasmsNuclear ProteinsTranscriptional ActivationTumor Protein p73Tumor Suppressor Protein p53DNA-Binding ProteinsNuclear ProteinsTP73 protein, humanTrp73 protein, mouseTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID17347683
PMCPMC1810568
OpenAlexW1967710981

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.