Evidence map›Paper›PMID 27172878›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016

P53 and the defenses against genome instability caused by transposons and repetitive elements.

Arnold J Levine, David T Ting, Benjamin D Greenbaum

Open access · hybridAbstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
16.4field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025
    Article
  8. Genes as Genome Stabilizers in Pluripotent Stem Cells.Advances in experimental medicine and biology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Inflammatory response to retrotransposons drives tumor drug resistance that can be prevented by reverse transcriptase inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Review
  18. Article
  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

3 authors at 3 institutions in 1 country.

Arnold J LevineInstitute for Advanced Study, School of Natural Sciences, The Simons Center for Systems Biology, Princeton, NJ, USA.
David T TingMassachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA, USA.
Benjamin D GreenbaumDepartment of Medicine, Hematology, and Medical Oncology, and Pathology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Center for Systems Biology · USHarvard University · USIcahn School of Medicine at Mount Sinai · US

Funding

Scientific ReagentsP01CA087497 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI STOCKWELL, BRENT R. · 2000 to 2021
$35.4M
Dana Farber/Harvard Cancer Consortium Career Development Program in Clinical OncologyK12CA087723 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI David Tsai Ting · 2002 to 2026
$17.9M
NCI NIH HHS K12 CA087723NCI NIH HHS P01 CA087497
6 · The paper itself

Abstract

The recent publication by Wylie et al. is reviewed, demonstrating that the p53 protein regulates the movement of transposons. While this work presents genetic evidence for a piRNA-mediated p53 interaction with transposons in Drosophila and zebrafish, it is herein placed in the context of a decade or so of additional work that demonstrated a role for p53 in regulating transposons and other repetitive elements. The line of thought in those studies began with the observation that transposons damage DNA and p53 regulates DNA damage. The presence of transposon movement can increase the rate of evolution in the germ line and alter genes involved in signal transduction pathways. Transposition can also play an important role in cancers where the p53 gene function is often mutated. This is particularly interesting as recent work has shown that de-repression of repetitive elements in cancer has important consequences for the immune system and tumor microenvironment.

Indexed as

DNA DamageDNA Transposable ElementsGenomic InstabilityRepetitive Sequences, Nucleic AcidTumor Suppressor Protein p53AnimalsDNAFemaleHumansMaleDNADNA Transposable ElementsTumor Suppressor Protein p53cancer biologycancer immunologyendogenous elementsgenome stabilityinnate immunityrepetitive elementstransposons

Identifiers

PMID27172878
PMCPMC5031199
OpenAlexW2385363635

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.