Evidence map›Paper›PMID 37449494›Full record

ReviewOncology reports2023

Mutant p53 in head and neck squamous cell carcinoma: Molecular mechanism of gain‑of‑function and targeting therapy (Review).

Minmin Li, Dongyuan Sun, Ning Song, Xi Chen, Xinyue Zhang, Wentian Zheng, Yang Yu, Chengbing Han

Open access · hybridAbstract readReview
In one paragraph

Review in Oncology reports, 2023. 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
6.0field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Modulation ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Transcriptome-based model for predicting radiotherapy response in HNSCC patients.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Minmin LiSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Dongyuan SunSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Ning SongSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Xi ChenSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Xinyue ZhangSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Wentian ZhengSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Yang YuSchool of Stomatology, Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Chengbing HanDepartment of Stomatology, First Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261000, P.R. China.
Weifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Head and neck squamous cell carcinoma (HNSCC) is one of the most widespread malignancies worldwide. p53, as a transcription factor, can play its role in tumor suppression by activating the expression of numerous target genes. However, p53 is one of the most commonly mutated genes, which frequently harbors missense mutations. These missense mutations are nucleotide substitutions that result in the substitution of an amino acid in the DNA binding domain. Most p53 mutations in HNSCC are missense mutations and the mutation rate of p53 reaches 65‑85%. p53 mutation not only inhibits the tumor suppressive function of p53 but also provides novel functions to facilitate tumor recurrence, called gain‑of‑function (GOF). The present study focused on the prevalence and clinical relevance of p53 mutations in HNSCC, and further described how mutant p53 accumulates. Moreover, mutant p53 in HNSCC can interact with proteins, RNA, and exosomes to exert effects on proliferation, migration, invasion, immunosuppression, and metabolism. Finally, several treatment strategies have been proposed to abolish the tumor‑promoting function of mutant p53; these strategies include reactivation of mutant p53 into wild‑type p53, induction of mutant p53 degradation, enhancement of the synthetic lethality of mutant p53, and treatment with immunotherapy. Due to the high frequency of p53 mutations in HNSCC, a further understanding of the mechanism of mutant p53 may provide potential applications for targeted therapy in patients with HNSCC.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsGain of Function MutationHumansMutationNeoplasm Recurrence, LocalSquamous Cell Carcinoma of Head and NeckTumor Suppressor Protein p53Tumor Suppressor Protein p53gain‑of‑functionhead and neck squamous cell carcinomamutant p53non‑coding RNAstherapeutic targettumor microenvironment

Identifiers

PMID37449494
PMCPMC10394732
OpenAlexW4383956251

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.