ArticleJournal of the National Cancer Institute2021
Epigenetic Age Acceleration and Chronic Health Conditions Among Adult Survivors of Childhood Cancer.
Article in Journal of the National Cancer Institute, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.
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Who cites it
54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 66 citations in OpenAlex.
- Accelerated epigenetic age in hypertension: a systematic review and meta-analysis.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Pooled it
- Association of Single-Nucleotide Variants in the Human Leukocyte Antigen and Other Loci With Childhood Hodgkin Lymphoma.JAMA network open · 2022Pooled it
- Genome-wide association studies identify novel genetic loci for epigenetic age acceleration among survivors of childhood cancer.Genome medicine · 2022Pooled it
- Potential for risk reduction of chronic health conditions through lifestyle in childhood cancer survivors.Nature communications · 2026Article
- Epigenetic age acceleration measures and chemotoxicity in older adults with early breast cancer.GeroScience · 2026Article
- Cancer Treatment-Related Cardiotoxicity among Survivors of Childhood Cancer: A Comparative and Integrated View of Multiple Measures of Biological Age Acceleration.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- Hypertension and epigenetic aging: socio-biological pathways of health disparity.Clinical epigenetics · 2026Article
- Neurometabolic correlates of accelerated aging and neurocognitive late effects in long-term survivors of pediatric hodgkin lymphoma and acute lymphoblastic leukemia.bioRxiv : the preprint server for biology · 2026Article
- Review
- Review
- KoMethylNet: a novel epigenetic clock based on neural network analysis of DNA methylation data and epigenetic age acceleration in a Korean population.BMC medicine · 2025Article
- Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer.Nature communications · 2025Article
- A Residual Approach to Estimate Biological Age from Gompertz Modeling.medRxiv : the preprint server for health sciences · 2025Article
- Epigenetic Age Acceleration Mediates Treatment Effects on Cardiometabolic and Cardiovascular Risk in Childhood Cancer Survivors.JACC. CardioOncology · 2025Article
- Unraveling the Genetic Associations with Epigenetic Age Acceleration in Childhood Cancer Survivors: Insights from GWAS Studies.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Accelerated Aging in Cancer and Cancer Treatment: Current Status of Biomarkers.Cancer medicine · 2025Review
- Sexual minority stress and epigenetic aging.Brain, behavior, and immunity · 2025Article
- Epidemiology of multimorbidity in childhood cancer survivors: a matched cohort study of inpatient hospitalisations in Western Australia.BJC reports · 2025Article
- Reevaluating Anti-Inflammatory Therapy: Targeting Senescence to Balance Anti-Cancer Efficacy and Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Association of phenotypic age acceleration with all-cause and cause-specific mortality among U.S. cancer survivors: a retrospective cohort study.BMC cancer · 2025Article
Corrections and comments
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Authors and funding
17 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundMounting evidence supports the occurrence of accelerating aging among long-term survivors of childhood cancer. We aimed to investigate epigenetic age acceleration (EAA) in survivors and evaluate associations between EAA, treatment exposures, health behaviors, and chronic health conditions (CHCs).
methodsGenome-wide methylation data were generated with Infinium EPIC BeadChip on blood-derived DNA from 2139 survivors and 282 frequency matched controls from the St Jude Lifetime Cohort Study. EAAs were estimated as residuals from a linear regression of epigenetic age (Levine's clock) against chronological age. Adjusted least square mean (ALSM) of EAA was calculated and compared between survivors and controls, across treatment exposures and health behaviors. Associations of EAA with 20 clinically assessed CHCs were evaluated with multivariable piecewise-exponential models. All statistical tests for P values below were 2-sided.
resultsEAA was statistically significantly higher in survivors than controls (ALSM = 0.63, 95% confidence interval [CI] = 0.26 to 1.01 vs -3.61, 95% CI = -4.43 to 2.80). In a multivariable model among survivors, statistically significantly higher EAA (P < .05) was observed in those exposed to chest radiotherapy, abdomen or pelvic radiotherapy, alkylating agents, glucocorticoids, or epipodophyllotoxins. Compared with survivors with favorable health behaviors (ALSM = 0.26, 95% CI=-0.36 to 0.87), EAA was statistically significantly higher among survivors with intermediate (ALSM = 1.07, 95% CI = 0.59 to 1.54) or unfavorable health behaviors (ALSM = 1.45, 95% CI = 0.60 to 2.30). In time-to-event analyses, statistically significant associations were identified between EAA tertiles and incidence of 7 CHCs: hypertension (3rd vs 1st tertile, relative rate [RR] = 1.83, 95% CI = 1.17 to 2.83), myocardial infarction (RR = 2.91, 95% CI = 1.27 to 7.21), obesity (RR = 1.39, 95% CI = 1.17 to 1.66), obstructive pulmonary deficit (RR = 1.86, 95% CI = 0.95 to 3.77), peripheral motor neuropathy (RR = 2.89, 95% CI = 1.24 to 6.97), peripheral sensory neuropathy (RR = 2.04, 95% CI = 0.99 to 4.26), and pulmonary diffusion deficits (RR = 2.75, 95% CI = 0.95 to 7.63).
conclusionsEAA is statistically significantly higher in survivors of childhood cancer than in noncancer controls and is associated with specific treatment exposures, unfavorable health behaviors, and presence of specific CHCs.
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