ReviewNature communications2025
The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.
Review in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed.
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- JMJD3-driven epigenetic reprogramming of p16Bone research · 2026Article
- Histone modifications across cancers: mechanisms, therapy and clinical translation.Molecular cancer · 2026Review
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Hierarchies of resistance to DNA damage response inhibitors: from pathway restoration to replication stress tolerance.Experimental hematology & oncology · 2026Review
- Common Signatures of Altered Gene Regulation and Invasiveness of Different Breast Cancer Cell Lines after Matrix Interface Crossing.Advanced healthcare materials · 2026Article
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
- Article
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- Targeting Tumour Heterogeneity through sequential timing of anti-hallmark combination therapies -a hypothesis for implementation.Frontiers in immunology · 2026Review
- Unravelling the nexus of non-coding RNAs in cancer stemness and therapeutic drug resistance.Frontiers in cell and developmental biology · 2026Review
- What Is Apoptosis and Why Is It Inhibited by the Most Important Tumor Suppressor (p53)?International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intra-tumor heterogeneity is a primary cause of therapeutic failure, driving tumor progression. Within tumors, diverse cell states coexist, maintained by a specific chromatin landscape that influences various cell functions, including cancer stemness. Among factors that induce chromatin changes affecting cell state fitness, DNA damage and its repair have emerged as significant contributors. This perspective examines recent advances that elucidate the interplay between DNA repair, epigenome, and cell plasticity. We discuss how epigenome affects DNA repair and, conversely, how DNA repair-induced chromatin changes influence cell plasticity. Finally, we discuss emerging concepts and highlight the therapeutic implications of these interconnected mechanisms.
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What OpenQuestion holds
Registered trials
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.