Evidence map›Paper›PMID 32414156›Full record

ReviewInternational journal of molecular sciences2020

P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.

Arjelle Decasa Agupitan, Paul Neeson, Scott Williams, Jason Howitt, Sue Haupt, Ygal Haupt

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
8.9field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  14. Phase I Trial of TTI-101, a First-in-Class Oral Inhibitor of STAT3, in Patients with Advanced Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  15. CENPF as a prognostic marker of glioma: unraveling the molecular mechanisms.Journal of cancer research and clinical oncology · 2025
    Article
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7 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Arjelle Decasa AgupitanTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Paul NeesonSir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia.
Scott WilliamsDivision of Radiation Oncology and Cancer Imaging, Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia.
Jason HowittSchool of Health Sciences, Swinburne University, Melbourne, VIC 3122, Australia.
Sue HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Ygal HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
The University of Melbourne · AUPeter MacCallum Cancer Centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Awareness of the importance of immunity in controlling cancer development triggered research into the impact of its key oncogenic drivers on the immune response, as well as their value as targets for immunotherapy. At the heart of tumour suppression is p53, which was discovered in the context of viral infection and now emerges as a significant player in normal and cancer immunity. Wild-type p53 (wt p53) plays fundamental roles in cancer immunity and inflammation. Mutations in p53 not only cripple wt p53 immune functions but also sinisterly subvert the immune function through its neomorphic gain-of-functions (GOFs). The prevalence of mutant p53 across different types of human cancers, which are associated with inflammatory and immune dysfunction, further implicates mutant p53 in modulating cancer immunity, thereby promoting tumorigenesis, metastasis and invasion. In this review, we discuss several mutant p53 immune GOFs in the context of the established roles of wt p53 in regulating and responding to tumour-associated inflammation, and regulating innate and adaptive immunity. We discuss the capacity of mutant p53 to alter the tumour milieu to support immune dysfunction, modulate toll-like receptor (TLR) signalling pathways to disrupt innate immunity and subvert cell-mediated immunity in favour of immune privilege and survival. Furthermore, we expose the potential and challenges associated with mutant p53 as a cancer immunotherapy target and underscore existing therapies that may benefit from inquiry into cancer p53 status.

Indexed as

Adaptive ImmunityGene Expression Regulation, NeoplasticHumansImmunity, InnateMutationNeoplasmsTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53cancer immunitycancer immunotherapygain of functioninflammationmutant p53

Identifiers

PMID32414156
PMCPMC7278985
OpenAlexW3024744974

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.