Evidence map›Paper›PMID 27048304›Full record

ReviewCold Spring Harbor perspectives in medicine2016

p53 in the DNA-Damage-Repair Process.

Ashley B Williams, Björn Schumacher

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 453 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
453citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

453 citing papers in PubMed, 1 synthesis or guideline pooled it, 813 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  13. Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Abemaciclib Inhibits Retinoblastoma Tumor Growth by Targeting CDK1/2.Investigative ophthalmology & visual science · 2026
    Article
  20. Review

393 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

2 authors at 2 institutions in 1 country.

Ashley B WilliamsMedical Faculty, Institute for Genome Stability in Ageing and Disease, University of Cologne, 50931 Cologne, Germany Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne (CMMC) and Systems Biology of Ageing Cologne, University of Cologne, 50931 Cologne, Germany.
Björn SchumacherMedical Faculty, Institute for Genome Stability in Ageing and Disease, University of Cologne, 50931 Cologne, Germany Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne (CMMC) and Systems Biology of Ageing Cologne, University of Cologne, 50931 Cologne, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

European Research Council 260383
6 · The paper itself

Abstract

The cells in the human body are continuously challenged by a variety of genotoxic attacks. Erroneous repair of the DNA can lead to mutations and chromosomal aberrations that can alter the functions of tumor suppressor genes or oncogenes, thus causing cancer development. As a central tumor suppressor, p53 guards the genome by orchestrating a variety of DNA-damage-response (DDR) mechanisms. Already early in metazoan evolution, p53 started controlling the apoptotic demise of genomically compromised cells. p53 plays a prominent role as a facilitator of DNA repair by halting the cell cycle to allow time for the repair machineries to restore genome stability. In addition, p53 took on diverse roles to also directly impact the activity of various DNA-repair systems. It thus appears as if p53 is multitasking in providing protection from cancer development by maintaining genome stability.

Indexed as

DNA DamageAnimalsCell CycleDNA RepairGenomic InstabilityHumansNeoplasmsTranscription, GeneticTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID27048304
PMCPMC4852800
OpenAlexW2341866865

What Socratic 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 Socratic graph.