ArticleBMC medicine2025
DNA methylation-based clocks, tobacco smoking, and lung cancer risk.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Epigenetic Age Acceleration as a Modifiable Public Health Target: A Systematic Review and Meta-Analysis of Environmental, Behavioral, and Social Determinants with Development of the MEAB-Index.International journal of molecular sciences · 2026Pooled it
- Epigenetic profiling of circulating cell-free DNA for early detection and minimal residual disease assessment in lung cancer: a focus on DNA methylation.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundBiological age, estimated by DNA methylation-based (DNAm) clocks, has been reported to be associated with lung cancer risk. However, the extent to which tobacco smoking behaviours can explain this association and the extent to which DNAm clocks and their components can inform risk assessment for lung cancer remains to be elucidated. This study aimed to evaluate the relationship between DNAm clocks, smoking, and lung cancer risk.
methodsWe analyzed four prospective cohorts (MCCS, Australia, 324 cases/324 controls; NSHDS, Sweden, 190 cases/190 controls; EPIC, Italy, 160 cases/107 controls; and NOWAC, Norway, 115 case/70 controls) with blood samples collected before lung cancer diagnosis. Study participants were restricted to those with a history of smoking. Incidence sampling was used to match one control to each of the lung cancer cases by cohort, sex, date of blood collection, age, and smoking status in MCCS and NSHDS. The risk discriminative performance of age-adjusted DNAm clocks and their components was compared with that of the Prostate, Lung, Colorectal, and Ovarian model 2012 (PLCO
resultsWe found several DNAm clocks positively associated with lung cancer risk (Hannum: OR = 1.13, 95% CI = 1.02-1.26; PhenoAge: OR = 1.25, 95% CI = 1.12-1.40; DunedinPACE: OR = 1.44, 95% CI = 1.29-1.62; PCGrimAge (a principal component-denoised GrimAge): OR = 1.79, 95% CI = 1.56-2.06), after adjustment for age and tobacco smoking. Tobacco smoking explained a modest proportion of variance in most age-adjusted DNAm clocks (R
conclusionsMethylation-based biological clocks capture epigenetic marks left by exposure to tobacco smoke, and some clocks may inform lung cancer risk assessment by complementing or replacing traditional prediction models.
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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.