ArticleAging and disease2025
Unveiling the Relation between Cellular Aging, Epigenetics and Cancer.
Article in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives.Journal of cellular and molecular medicine · 2026Review
- Novel Exploratory Transcriptomic Candidates as Biomarkers and Cancer Hallmark Fingerprints for Ovarian Endometroid and Clear Cell Carcinomas in Women.Antioxidants (Basel, Switzerland) · 2026Article
- From linear methylation to spatial metabolic control: Rethinking DNMT1 targeting in MASLD: Letter to the editor on "DNMT1 facilitates the progression of MASLD by impeding transcription mediated by HNF4α and PPARα".Clinical and molecular hepatology · 2026Article
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This Editorial article intends to unravel the relationships among cellular aging, epigenetic changes, and tumorigenesis, thereby offering perspectives that could improve therapeutic approaches in cancer management and promote future research on these topics. Furthermore, selected fundamental principles concerning cellular aging will be presented to elucidate how this process contributes to the comprehension of tumorigenesis. As humans age, there is a progressive decline in physiological functions, which significantly increases the risk of cancer. Epigenetic alterations-heritable yet reversible modifications of the genome without changes in DNA sequence-play a pivotal role in both aging and tumorigenesis. Age-associated epigenetic drift, involving widespread DNA methylation changes, histone modification shifts, and chromatin remodelling, disrupts normal gene regulatory networks, leading to genomic instability and impaired cellular homeostasis. Additionally, the accumulation of senescent cells, driven by epigenetic dysregulation, fosters a pro-inflammatory environment that can promote tumorigenesis. Moreover, the epigenetic landscape of aged tissues resembles that of cancerous tissues, suggesting that aging establishes a permissive environment for malignant transformation. Understanding the interplay between aging, epigenetic regulation, and cancer is critical for the development of preventive strategies and novel therapeutics. Epigenetic reprogramming technologies, aiming to restore youthful epigenetic states, hold promise for delaying aging and reducing cancer incidence. However, challenges remain in selectively targeting pathogenic epigenetic changes without disrupting essential cellular functions.
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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.