Correlation of an epigenetic mitotic clock with cancer risk
Open accessAbstract
BACKGROUND: Variation in cancer risk among somatic tissues has been attributed to variations in the underlying rate of stem cell division. For a given tissue type, variable cancer risk between individuals is thought to be influenced by extrinsic factors which modulate this rate of stem cell division. To date, no molecular mitotic clock has been developed to approximate the number of stem cell divisions in a tissue of an individual and which is correlated with cancer risk. RESULTS: Here, we integrate mathematical modeling with prior biological knowledge to construct a DNA methylation-based age-correlative model which approximates a mitotic clock in both normal and cancer tissue. By focusing on promoter CpG sites that localize to Polycomb group target genes that are unmethylated in 11 different fetal tissue types, we show that increases in DNA methylation at these sites defines a tick rate which correlates with the estimated rate of stem cell division in normal tissues. Using matched DNA methylation and RNA-seq data, we further show that it correlates with an expression-based mitotic index in cancer tissue. We demonstrate that this mitotic-like clock is universally accelerated in cancer, including pre-cancerous lesions, and that it is also accelerated in normal epithelial cells exposed to a major carcinogen. CONCLUSIONS: Unlike other epigenetic and mutational clocks or the telomere clock, the epigenetic clock proposed here provides a concrete example of a mitotic-like clock which is universally accelerated in cancer and precancerous lesions.
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Yang et al. built an epigenetic clock associated with the number of cell divisions by pre-selecting CpG sites that had low methylation in fetal tissue and increased methylation throughout adulthood and that mapped to Polycomb group target promoters.
“In 2016, Yang et al.62 built an epigenetic clock associated with the number of cell divisions by pre-selecting CpG sites that had low levels of methylation in fetal tissue and increased methylation levels throughout adulthood and that mapped to Polycomb group target (PCGT) promoters, before training a sparse linear model.”
From Measuring biological age using omics data (2022) · cites this paper as [62]
The Yang et al. clock uniquely detected precancerous tissue samples to be age accelerated.
“Strikingly, this clock uniquely detected precancerous tissue samples to be age accelerated.”
From Measuring biological age using omics data (2022) · cites this paper as [62]
Yang et al. and Lu et al. trained clocks on cellular features - mitotic cell division and telomere length, respectively - to develop models with specific sensitivity for these aspects of cellular ageing.
“Yang et al.62 and Lu et al.167 took a different approach and trained clocks on cellular features — mitotic cell division and telomere length, respectively — to develop models with specific sensitivity for these aspects of cellular ageing.”
From Measuring biological age using omics data (2022) · cites this paper as [62]
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- Authors
- Yang, Z., Wong, A., Kuh, D., Paul, D. S., Rakyan, V. K., Leslie, R. D., Zheng, S. C., Widschwendter, M., Beck, S., & Teschendorff, A. E.
- Affiliations
- Chinese Academy of Sciences (CN)
- MRC Unit for Lifelong Health and Ageing (GB)
- University College London (GB)
- Queen Mary University of London (GB)
- Corresponding author
- Teschendorff, Andrew E.
- ORCID
- Venue
- Genome Biology
- Published
- 2016-10-03
- Volume
- 17
- Issue
- 1
- Pages
- 205-205
- ISSN
- 1465-6906 (ISSN-L)
- 1474-760X
- PMC
- PMC5046977
- OpenAlex
- W2529317472
- Cited by
- 325
- References
- 71
- Citations by year
- 2026: 31 · 2025: 52 · 2024: 43 · 2023: 40 · 2022: 53 · 2021: 32 · 2020: 25 · 2019: 17 · 2018: 18 · 2017: 12 · 2016: 1
- FWCI
- 8.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Genome biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion, cc-by)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Apollo (cc-by)
- Funders
- Royal Society (NAF 164914)
- National Science Foundation of China (NSFC 31571359)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- epigenetic clocks, DNA methylation, stem cell division, cancer risk, promoter CpG sites, fetal tissue, carcinogen exposure, precancerous lesions, cancer risk stratification
- MeSH terms
- Aging, Humans, Mitosis, Mitotic Index, Models, Theoretical, Neoplasms, Promoter Regions, Genetic, Neoplastic Stem Cells, Gene Expression Regulation, Neoplastic, CpG Islands, DNA Methylation, Epigenesis, Genetic, High-Throughput Nucleotide Sequencing, Polycomb-Group Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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