Evidence map›Paper›PMID 22239435›Full record

ReviewExpert opinion on therapeutic targets2012

Targeting the p53 signaling pathway in cancer therapy - the promises, challenges and perils.

Alexander H Stegh

Abstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 196 citations in OpenAlex.

  1. Recombinant Human Adenovirus-Medicina (Kaunas, Lithuania) · 2021
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024
    Review
  7. Allicin: a promising modulator of apoptosis and survival signaling in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Food & nutrition research · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

47 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution.

Alexander H SteghFeinberg School of Medicine, The Robert H. Lurie Comprehensive Cancer Center, Davee Department of Neurology, Chicago, IL 60611, USA. stegh@northwestern.edu
Robert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

Theranostic Magnetic Nanostructures for the Molecular Imaging of CancerU54CA151880 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WOLOSCHAK, GAYLE E. · 2010 to 2014
$11.5M
The Role of Bcl2L12 in the Genesis of Malignant GliomaR00CA129172 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STEGH, ALEXANDER H. · 2009 to 2011
$740k
NCI NIH HHS R00 CA129172NCI NIH HHS R00CA129172NCI NIH HHS U54 CA151880NCI NIH HHS U54CA151880
6 · The paper itself

Abstract

introductionResearch over the past three decades has identified p53 as a multi-functional transcription factor. p53 influences myriad, highly diverse cellular processes, and represents one of the most important and extensively studied tumor suppressors. Activated by various stresses, p53 blocks cancer progression by provoking transient or permanent growth arrest, by enabling DNA repair, or by advancing cellular death programs. This anti-cancer activity profile, together with genomic and mutational analyses documenting inactivation of p53 in more than 50% of human cancers, motivated drug development efforts to (re-) activate p53 in established tumors. AREAS COVERED: The complexities of p53 signaling in cancer are summarized, including current strategies and challenges to restore p53's tumor suppressive function in established tumors, to inactivate p53 inhibitors, and to restore wild type function of p53 mutant proteins. EXPERT OPINION: p53 represents an attractive target for the development of anti-cancer therapies. Whether p53 is 'druggable', however, remains an area of active research and discussion, as p53 has pro-survival functions and chronic p53 activation accelerates aging, which may compromise the long-term homeostasis of an organism. The complex biology and dual functions of p53 in cancer prevention and age-related cellular responses pose significant challenges to the development of p53-targeting cancer therapies.

Indexed as

AnimalsAntineoplastic AgentsGenetic TherapyHumansNeoplasmsSignal TransductionTumor Suppressor Protein p53Antineoplastic AgentsTumor Suppressor Protein p53

Identifiers

PMID22239435
PMCPMC3291789
OpenAlexW1980250100

What OpenQuestion holds

Textmetadata
LicenceTDM
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.