Evidence map›Paper›PMID 39612910›Full record

ReviewRedox biology2024

Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.

Geoffrey Balamurli, Angeline Qiu Xia Liew, Wee Wei Tee, Shazib Pervaiz

Abstract readReview
In one paragraph

Review in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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.

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

17 citing papers in PubMed.

  1. Review
  2. On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. The Role of Renal Cell Senescence in Diabetic Kidney Disease: Mechanisms and Therapeutic Advances.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  17. Review
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.

Geoffrey BalamurliDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore; NUS Centre for Cancer Research (N2CR), Yong Loo Lin School of Medicine, NUS, Singapore; Chromatin Dynamics and Disease Epigenetics Lab, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A∗STAR), Singapore.
Angeline Qiu Xia LiewDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore; Integrative Science and Engineering Programme (ISEP), NUS Graduate School (NUSGS), NUS, Singapore.
Wee Wei TeeDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore; NUS Centre for Cancer Research (N2CR), Yong Loo Lin School of Medicine, NUS, Singapore; Chromatin Dynamics and Disease Epigenetics Lab, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A∗STAR), Singapore.
Shazib PervaizDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore; NUS Centre for Cancer Research (N2CR), Yong Loo Lin School of Medicine, NUS, Singapore; Integrative Science and Engineering Programme (ISEP), NUS Graduate School (NUSGS), NUS, Singapore; NUS Medicine Healthy Longevity Program, NUS, Singapore; National University Cancer Institute, National University Health System, Singapore. Electronic address: phssp@nus.edu.sg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is accumulating evidence indicating a close crosstalk between key molecular events regulating cell growth and proliferation, which could profoundly impact carcinogenesis and its progression. Here we focus on reviewing observations highlighting the interplay between epigenetic modifications, irreversible cell cycle arrest or senescence, and cellular redox metabolism. Epigenetic alterations, such as DNA methylation and histone modifications, dynamically influence tumour transcriptome, thereby impacting tumour phenotype, survival, growth and spread. Interestingly, the acquisition of senescent phenotype can be triggered by epigenetic changes, acting as a double-edged sword via its ability to suppress tumorigenesis or by facilitating an inflammatory milieu conducive for cancer progression. Concurrently, an aberrant redox metabolism, which is a function of the balance between reactive oxygen species (ROS) generation and intracellular anti-oxidant defences, influences signalling cascades and genomic stability in cancer cells by serving as a critical link between epigenetics and senescence. Recognizing this intricate interconnection offers a nuanced perspective for therapeutic intervention by simultaneously targeting specific epigenetic modifications, modulating senescence dynamics, and restoring redox homeostasis.

Indexed as

Cellular SenescenceEpigenesis, GeneticNeoplasmsOxidation-ReductionReactive Oxygen SpeciesAnimalsDNA MethylationGene Expression Regulation, NeoplasticHumansReactive Oxygen SpeciesCancerEpigenetic modificationsRedox statusSASPSenescence

Identifiers

PMID39612910
PMCPMC11629570

What OpenQuestion holds

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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.