Evidence map›Paper›PMID 38311377›Full record

ReviewCancer communications (London, England)2024

Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.

Bin Song, Ping Yang, Shuyu Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Cancer communications (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
17.5field-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

54 citing papers in PubMed, 75 citations in OpenAlex.

  1. Camrelizumab, Apatinib, and Radiotherapy in Locally Advanced, Unresectable Hepatocellular Carcinoma: A Phase II Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Trial
  2. Review
  3. Time- and dose-dependent regulation of circular RNAs in the response of triple-negative breast cancer cells to ionizing radiation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  4. Targeting glutathione metabolism for tumor radiosensitization (Review).International journal of molecular medicine · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

3 authors at 2 institutions in 1 country.

Bin SongLaboratory of Radiation Medicine, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, P. R. China.
Ping YangLaboratory of Radiation Medicine, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, P. R. China.
Shuyu ZhangLaboratory of Radiation Medicine, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, P. R. China.ORCID 0000-0003-1419-3635
Sichuan University · CNChina National Nuclear Corporation · CN

Funding

National Natural Science Foundation of China 82073477the Young Talent Project of China National Nuclear Corporation, and Scientific Fund for Distinguished Young Scholars in Sichuan Province 2022JDJQ0051
6 · The paper itself

Abstract

Cancer is a leading cause of death worldwide. Targeted therapies aimed at key oncogenic driver mutations in combination with chemotherapy and radiotherapy as well as immunotherapy have benefited cancer patients considerably. Tumor protein p53 (TP53), a crucial tumor suppressor gene encoding p53, regulates numerous downstream genes and cellular phenotypes in response to various stressors. The affected genes are involved in diverse processes, including cell cycle arrest, DNA repair, cellular senescence, metabolic homeostasis, apoptosis, and autophagy. However, accumulating recent studies have continued to reveal novel and unexpected functions of p53 in governing the fate of tumors, for example, functions in ferroptosis, immunity, the tumor microenvironment and microbiome metabolism. Among the possibilities, the evolutionary plasticity of p53 is the most controversial, partially due to the dizzying array of biological functions that have been attributed to different regulatory mechanisms of p53 signaling. Nearly 40 years after its discovery, this key tumor suppressor remains somewhat enigmatic. The intricate and diverse functions of p53 in regulating cell fate during cancer treatment are only the tip of the iceberg with respect to its equally complicated structural biology, which has been painstakingly revealed. Additionally, TP53 mutation is one of the most significant genetic alterations in cancer, contributing to rapid cancer cell growth and tumor progression. Here, we summarized recent advances that implicate altered p53 in modulating the response to various cancer therapies, including chemotherapy, radiotherapy, and immunotherapy. Furthermore, we also discussed potential strategies for targeting p53 as a therapeutic option for cancer.

Indexed as

NeoplasmsTumor Suppressor Protein p53FriendsGenes, p53HumansMutationTumor MicroenvironmentTumor Suppressor Protein p53cancerchemotherapydrug targetingimmunotherapyp53tumor suppressor

Identifiers

PMID38311377
PMCPMC10958678
OpenAlexW4392735609

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.