Evidence map›Paper›PMID 29992419›Full record

ReviewMammalian genome : official journal of the International Mammalian Genome Society2018

A mouse model of the Δ133p53 isoform: roles in cancer progression and inflammation.

Marina Kazantseva, Sunali Mehta, Ramona A Eiholzer, Noelyn Hung, Anna Wiles, Tania L Slatter, Antony W Braithwaite

Abstract readReview
PubMed Publisher
In one paragraph

Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. IntronicCancers · 2020
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Introduction to Mammalian Genome special issue: inflammation and immunity in cancer.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    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

7 authors.

Marina KazantsevaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Sunali MehtaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Ramona A EiholzerDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Noelyn HungDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Anna WilesDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Tania L SlatterDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Antony W BraithwaiteDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. antony.braithwaite@otago.ac.nz.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review paper outlines studies on the Δ122p53 mouse, a model of the human Δ133p53 isoform, together with studies in other model organisms, cell culture, and where available, clinical investigations. In general, these studies imply that, in contrast to the canonical p53 tumor suppressor, Δ133p53 family members have oncogenic capability. Δ122p53 is multi-functional, conferring survival and proliferative advantages on cells, promoting invasion, metastasis and vascularization, as does Δ133p53. Cancers with high levels of Δ133p53 often have poor prognosis. Δ122p53 mediates its effects through the JAK-STAT and RhoA-ROCK signaling pathways. We propose that Δ133p53 isoforms have evolved as inflammatory signaling molecules to deal with the consequent tissue damage of p53 activation. However, if sustained expression of the isoforms occur, pathologies may result.

Indexed as

Disease Models, AnimalAnimalsDisease ProgressionHumansInflammationMiceNeoplasmsProtein IsoformsSignal TransductionTumor Suppressor Protein p53Protein IsoformsTumor Suppressor Protein p53

Identifiers

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.