Evidence map›Paper›PMID 26068791›Full record

ArticleCell death & disease2015

Δ122p53, a mouse model of Δ133p53α, enhances the tumor-suppressor activities of an attenuated p53 mutant.

T L Slatter, N Hung, S Bowie, H Campbell, C Rubio, D Speidel, M Wilson, M Baird, J A Royds, A W Braithwaite

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Review
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  8. A mouse model of the Δ133p53 isoform: roles in cancer progression and inflammation.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. p53 Isoforms: Key Regulators of the Cell Fate Decision.Cold Spring Harbor perspectives in medicine · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. 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

10 authors.

T L SlatterDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
N HungDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
S BowieDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
H CampbellChildren's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
C RubioChildren's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
D SpeidelChildren's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia.
M WilsonDepartment of Microbiology and Immunology, School of Medical Sciences, University of Otago, Dunedin, New Zealand.
M BairdDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
J A RoydsDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
A W Braithwaite1] Department of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand [2] Children's Medical Research Institute, University of Sydney, Westmead, New South Wales, Australia [3] Maurice Wilkins Centre for BioDiscovery, University of Otago, Dunedin, New Zealand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence suggests the Δ133p53α isoform may function as an oncogene. It is overexpressed in many tumors, stimulates pathways involved in tumor progression, and inhibits some activities of wild-type p53, including transactivation and apoptosis. We hypothesized that Δ133p53α would have an even more profound effect on p53 variants with weaker tumor-suppressor capability. We tested this using a mouse model heterozygous for a Δ133p53α-like isoform (Δ122p53) and a p53 mutant with weak tumor-suppressor function (mΔpro). The Δ122p53/mΔpro mice showed a unique survival curve with a wide range of survival times (92-495 days) which was much greater than mΔpro/- mice (range 120-250 days) and mice heterozygous for the Δ122p53 and p53 null alleles (Δ122p53/-, range 78-150 days), suggesting Δ122p53 increased the tumor-suppressor activity of mΔpro. Moreover, some of the mice that survived longest only developed benign tumors. In vitro analyses to investigate why some Δ122p53/mΔpro mice were protected from aggressive tumors revealed that Δ122p53 stabilized mΔpro and prolonged the response to DNA damage. Similar effects of Δ122p53 and Δ133p53α were observed on wild-type of full-length p53, but these did not result in improved biological responses. The data suggest that Δ122p53 (and Δ133p53α) could offer some protection against tumors by enhancing the p53 response to stress.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cysteine Proteinase InhibitorsDisease Models, AnimalDNA DamageInterferon-gammaInterleukin-6LeupeptinsLymphoma, B-CellMaleMiceAntineoplastic Agentsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCyclin-Dependent Kinase Inhibitor p21Cysteine Proteinase InhibitorsInterferon-gammaInterleukin-6LeupeptinsMdm2 protein, mouseProtein IsoformsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID26068791
PMCPMC4669831

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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.