Evidence map›Paper›PMID 21188172›Full record

ReviewJournal of biomedicine & biotechnology2011

p53: the attractive tumor suppressor in the cancer research field.

Toshinori Ozaki, Akira Nakagawara

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.8field-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

47 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Review
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  7. Frontiers in cell and developmental biology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Oncology letters · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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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

2 authors at 1 institution in 1 country.

Toshinori OzakiLaboratory of Anti-Tumor Research, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan.
Akira Nakagawara
Chiba Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle arrest, DNA repair, and apoptotic cell death. In response to cellular stresses such as DNA damage, p53 is activated and promotes cell cycle arrest followed by the replacement of DNA lesions and/or apoptotic cell death. Therefore, p53 is able to maintain the genomic integrity to prevent the accumulation of genetic alterations, and thus stands at a crossroad between cell survival and cell death. In this paper, we describe a variety of molecular mechanisms behind the regulation of p53.

Indexed as

Genes, p53AnimalsHumansMiceMutationNeoplasmsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID21188172
PMCPMC3004423
OpenAlexW1988125845

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.