Evidence map›Paper›PMID 26858938›Full record

ReviewFrontiers in oncology2016

Mutant p53 Drives Cancer by Subverting Multiple Tumor Suppression Pathways.

Sue Haupt, Dinesh Raghu, Ygal Haupt

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Oncology letters · 2018
    Article
  16. Current urology · 2018
    Article
  17. Article
  18. New therapeutic strategies to treat human cancers expressing mutant p53 proteins.Journal of experimental & clinical cancer research : CR · 2018
    Review
  19. Review
  20. Molecularly targeted therapies for p53-mutant cancers.Cellular and molecular life sciences : CMLS · 2017
    Review
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.

Sue HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Department of Pathology, The University of Melbourne, Parkville, VIC, Australia.
Dinesh RaghuTumour Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia.
Ygal HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Department of Pathology, The University of Melbourne, Parkville, VIC, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53 normally acts as a brake to halt damaged cells from perpetrating their genetic errors into future generations. If p53 is disrupted by mutation, it may not only lose these corrective powers, but counterproductively acquire new capacities that drive cancer. A newly emerging manner in which mutant p53 executes its cancer promoting functions is by harnessing key proteins, which normally partner with its wild type, tumor-inhibiting counterpart. In association with the subverted activities of these protein partners, mutant p53 is empowered to act across multiple fundamental cellular pathways (regulating cell division and metabolism) and corrupt them to become cancer promoting.

Indexed as

cell cyclegain of functionmetabolismp53 mutationstranscriptional regulation

Identifiers

PMID26858938
PMCPMC4728204

What OpenQuestion holds

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Registered trials

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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.