Evidence map›Paper›PMID 29242642›Full record

ReviewNature reviews. Cancer2018

Targeting mutant p53 for efficient cancer therapy.

Vladimir J N Bykov, Sofi E Eriksson, Julie Bianchi, Klas G Wiman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 525 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
525citing papers in PubMed, 4 pooled it
32.4field-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

525 citing papers in PubMed, 4 syntheses or guidelines pooled it, 893 citations in OpenAlex.

  1. Impact of TP53 somatic mutations on prognosis in endometrial cancer: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  5. Trial
  6. Article
  7. Review
  8. Determinants of CBiomolecules · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  13. Article
  14. RiboScreenBiomedicines · 2026
    Review
  15. Review
  16. Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  17. Article
  18. Reactivation ofInternational journal of molecular sciences · 2026
    Article
  19. Article
  20. IHC p53 Performance in NordiQC: Recalibration of IHC Assays is Needed.Applied immunohistochemistry & molecular morphology : AIMM · 2026
    Article

465 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

4 authors at 1 institution in 1 country.

Vladimir J N BykovKarolinska Institutet, Department of Oncology-Pathology, Cancer Center Karolinska (CCK), SE-171 77 Stockholm, Sweden.
Sofi E ErikssonKarolinska Institutet, Department of Oncology-Pathology, Cancer Center Karolinska (CCK), SE-171 77 Stockholm, Sweden.
Julie BianchiKarolinska Institutet, Department of Oncology-Pathology, Cancer Center Karolinska (CCK), SE-171 77 Stockholm, Sweden.
Klas G WimanKarolinska Institutet, Department of Oncology-Pathology, Cancer Center Karolinska (CCK), SE-171 77 Stockholm, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour suppressor gene TP53 is the most frequently mutated gene in cancer. Wild-type p53 can suppress tumour development by multiple pathways. However, mutation of TP53 and the resultant inactivation of p53 allow evasion of tumour cell death and rapid tumour progression. The high frequency of TP53 mutation in tumours has prompted efforts to restore normal function of mutant p53 and thereby trigger tumour cell death and tumour elimination. Small molecules that can reactivate missense-mutant p53 protein have been identified by different strategies, and two compounds are being tested in clinical trials. Novel approaches for targeting TP53 nonsense mutations are also underway. This Review discusses recent progress in pharmacological reactivation of mutant p53 and highlights problems and promises with these strategies.

Indexed as

AnimalsAntineoplastic AgentsCell DeathHumansMutant ProteinsMutationNeoplasmsTumor Suppressor Protein p53Antineoplastic AgentsMutant ProteinsTumor Suppressor Protein p53

Identifiers

PMID29242642
OpenAlexW2772062014

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.