Evidence map›Paper›PMID 30538286›Full record

ReviewCell death and differentiation2019

Mutant p53 as a guardian of the cancer cell.

Fiamma Mantovani, Licio Collavin, Giannino Del Sal

Registry-linked trialAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07150416 (A Single-Arm Clinical Study of Nebulized Inhalation of Recombinant Human p53 Adenovirus Injection), which is not on this map. Cited by 475 papers.

0numbers the graph read from it
0cells of the map it votes in
475citing 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.

NCT07150416 phase2not yet recruitingnot on this mapstarted 2025, after this paper: background citation

A Single-Arm Clinical Study of Nebulized Inhalation of Recombinant Human p53 Adenovirus Injection (Gendicine) for Treatment of Multiple Ground-Glass Lung Nodules

TypeinterventionalSponsorThe First Affiliated Hospital of Guangzhou Medical UniversityRan2025 to 2027Enrolled38ConditionsMultiple Pulmonary Ground-Glass Nodules, Lung Neoplasms, Precancerous ConditionsArmsRecombinant Human Ad-p53 Injection
3 · Its place in the literature

Who cites it

475 citing papers in PubMed.

  1. Trial
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  6. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  11. Assessing the significance of CCNE1 overexpression in triple negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  12. Review
  13. ComplexInternational journal of molecular sciences · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Reactivation ofInternational journal of molecular sciences · 2026
    Article
  20. Article

415 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

3 authors.

Fiamma MantovaniLaboratorio Nazionale CIB (LNCIB), AREA Science Park, Trieste, Italy.
Licio CollavinLaboratorio Nazionale CIB (LNCIB), AREA Science Park, Trieste, Italy.ORCID http://orcid.org/0000-0001-6815-5381
Giannino Del SalLaboratorio Nazionale CIB (LNCIB), AREA Science Park, Trieste, Italy. giannino.delsal@lncib.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forty years of research have established that the p53 tumor suppressor provides a major barrier to neoplastic transformation and tumor progression by its unique ability to act as an extremely sensitive collector of stress inputs, and to coordinate a complex framework of diverse effector pathways and processes that protect cellular homeostasis and genome stability. Missense mutations in the TP53 gene are extremely widespread in human cancers and give rise to mutant p53 proteins that lose tumor suppressive activities, and some of which exert trans-dominant repression over the wild-type counterpart. Cancer cells acquire selective advantages by retaining mutant forms of the protein, which radically subvert the nature of the p53 pathway by promoting invasion, metastasis and chemoresistance. In this review, we consider available evidence suggesting that mutant p53 proteins can favor cancer cell survival and tumor progression by acting as homeostatic factors that sense and protect cancer cells from transformation-related stress stimuli, including DNA lesions, oxidative and proteotoxic stress, metabolic inbalance, interaction with the tumor microenvironment, and the immune system. These activities of mutant p53 may explain cancer cell addiction to this particular oncogene, and their study may disclose tumor vulnerabilities and synthetic lethalities that could be exploited for hitting tumors bearing missense TP53 mutations.

Indexed as

OncogenesCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMutant ProteinsMutation, MissenseNeoplasmsTumor MicroenvironmentTumor Suppressor Protein p53Mutant ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30538286
PMCPMC6329812

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.