Evidence map›Paper›PMID 18832062›Full record

ReviewGenes & development2008

The jury is in: p73 is a tumor suppressor after all.

Jennifer M Rosenbluth, Jennifer A Pietenpol

Open access · diamondAbstract readReviewComment
PubMed Publisher
In one paragraph

Review in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. MDM2, MDMX, and p73 regulate cell-cycle progression in the absence of wild-type p53.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  4. Article
  5. p53 shades of Hippo.Cell death and differentiation · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. TAp73 transcriptionally represses BNIP3 expression.Cell cycle (Georgetown, Tex.) · 2015
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jennifer M RosenbluthDepartment of Biochemistry, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennesee 37232, USA.
Jennifer A Pietenpol
Vanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While p53 has been extensively characterized as a tumor suppressor, it has been more difficult to determine whether p63 and/or p73 play a similar role. Every system in which these family members have been studied, from cells to animal models to human tissues, seems to create more questions than answers. Tomasini and colleagues (2677-2691) demonstrate that one isoform of p73 is responsible for preventing tumor formation in vivo, providing critical validation of an isoform-based model of p73 function.

Indexed as

Genes, Tumor SuppressorAnimalsDNA-Binding ProteinsFemaleGenomic InstabilityHumansInfertilityMaleMiceMice, KnockoutModels, BiologicalMutationNeoplasmsNuclear ProteinsProtein IsoformsSignal TransductionDNA-Binding ProteinsNuclear ProteinsProtein IsoformsTP73 protein, humanTrp73 protein, mouseTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID18832062
OpenAlexW2154111880

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.