Evidence map›Paper›PMID 30892598›Full record

ReviewJournal of molecular cell biology2019

p53 as a hub in cellular redox regulation and therapeutic target in cancer.

Sofi E Eriksson, Sophia Ceder, Vladimir J N Bykov, Klas G Wiman

Open access · goldAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.3field-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

64 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
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  10. Germline-Somatic Interactions in BRCA-Associated Cancers: Unique Molecular Profiles and Clinical Outcomes Linking ATM to TP53 Synthetic Essentiality.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
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  19. Targeting ROS in cancer: rationale and strategies.Nature reviews. Drug discovery · 2024
    Review
  20. Article

4 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.

Sofi E ErikssonKarolinska Institutet, Department of Oncology-Pathology, BioClinicum, Stockholm, Sweden.
Sophia CederKarolinska Institutet, Department of Oncology-Pathology, BioClinicum, Stockholm, Sweden.
Vladimir J N BykovKarolinska Institutet, Department of Oncology-Pathology, BioClinicum, Stockholm, Sweden.
Klas G WimanKarolinska Institutet, Department of Oncology-Pathology, BioClinicum, Stockholm, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TP53 tumor suppressor gene encodes a DNA-binding transcription factor that regulates multiple cellular processes including cell growth and cell death. The ability of p53 to bind to DNA and activate transcription is tightly regulated by post-translational modifications and is dependent on a reducing cellular environment. Some p53 transcriptional target genes are involved in regulation of the cellular redox homeostasis, e.g. TIGAR and GLS2. A large fraction of human tumors carry TP53 mutations, most commonly missense mutations that lead to single amino acid substitutions in the core domain. Mutant p53 proteins can acquire so called gain-of-function activities and influence the cellular redox balance in various ways, for instance by binding of the Nrf2 transcription factor, a major regulator of cellular redox state. The DNA-binding core domain of p53 has 10 cysteine residues, three of which participate in holding a zinc atom that is critical for p53 structure and function. Several novel compounds that refold and reactivate missense mutant p53 bind to specific p53 cysteine residues. These compounds can also react with other thiols and target components of the cellular redox system, such as glutathione. Dual targeting of mutant p53 and redox homeostasis may allow more efficient treatment of cancer.

Indexed as

AntioxidantsDNAHumansMutation, MissenseNeoplasmsOxidative StressSmall Molecule LibrariesSulfhydryl CompoundsTumor MicroenvironmentTumor Suppressor Protein p53AntioxidantsDNASmall Molecule LibrariesSulfhydryl CompoundsTumor Suppressor Protein p53cancer therapymutationNrf2oxidative stressp53redox regulationthiols

Identifiers

PMID30892598
PMCPMC6734141
OpenAlexW2911745809

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.