SynthesisGenome medicine2022
Genome-wide association studies identify novel genetic loci for epigenetic age acceleration among survivors of childhood cancer.
Synthesis in Genome medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Genome-wide association studies identify novel genetic loci for epigenetic age acceleration among survivors of childhood cancer.Genome medicine · 2022Pooled it
- Integrating biological aging into clinical practice: a review and path forward for precision longevity medicine.GeroScience · 2026Review
- A genome-wide association study identifies Asian-specific genetic susceptibility for epigenetic age acceleration.GeroScience · 2026Article
- Dissecting shared genetic architecture between pan-cancer and aging-related traits: a genome-wide cross-trait analysis.Biogerontology · 2026Article
- Article
- Unraveling the Genetic Associations with Epigenetic Age Acceleration in Childhood Cancer Survivors: Insights from GWAS Studies.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Genetic and epigenetic bases of long-term adverse effects of childhood cancer therapy.Nature reviews. Cancer · 2025Review
- Applicability of epigenetic age models to next-generation methylation arrays.Genome medicine · 2024Article
- A comprehensive map of the aging blood methylome in humans.Genome biology · 2024Article
- Article
- Race and Ethnicity, Socioeconomic Factors, and Epigenetic Age Acceleration in Survivors of Childhood Cancer.JAMA network open · 2024Article
- Health-related quality of life and DNA methylation-based aging biomarkers among survivors of childhood cancer.Journal of the National Cancer Institute · 2024Article
- CheekAge: a next-generation buccal epigenetic aging clock associated with lifestyle and health.GeroScience · 2024Article
- Article
- Mortality After Major Cardiovascular Events in Survivors of Childhood Cancer.Journal of the American College of Cardiology · 2024Article
- Gene-Level Analysis of Anthracycline-Induced Cardiomyopathy in Cancer Survivors: A Report From COG-ALTE03N1, BMTSS, and CCSS.JACC. CardioOncology · 2023Article
- Epigenetic Age in Peripheral Blood Among Children, Adolescent, and Adult Survivors of Childhood Cancer.JAMA network open · 2023Article
- Distinct DNA methylation signatures associated with blood lipids as exposures or outcomes among survivors of childhood cancer: a report from the St. Jude lifetime cohort.Clinical epigenetics · 2023Article
- Inflammatory biomarkers after an exercise intervention in childhood acute lymphoblastic leukemia survivors.EJHaem · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 2 institutions in 3 countries.
Funding
Abstract
backgroundIncreased epigenetic age acceleration (EAA) in survivors of childhood cancer is associated with specific treatment exposures, unfavorable health behaviors, and presence of certain chronic health conditions. To better understand inter-individual variability, we investigated the genetic basis underlying EAA.
methodsGenome-wide association studies of EAA based on multiple epigenetic clocks (Hannum, Horvath, PhenoAge, and GrimAge) were performed. MethylationEPIC BeadChip array and whole-genome sequencing data were generated with blood-derived DNA from participants in the St. Jude Lifetime Cohort Study (discovery: 2138 pre-existing and 502 newly generated data, all survivors; exploratory: 282 community controls). Linear regression models were fit for each epigenetic age against the allelic dose of each genetic variant, adjusting for age at sampling, sex, and cancer treatment exposures. Fixed-effects meta-analysis was used to combine summary statistics from two discovery data sets. LD (Linkage disequilibrium) score regression was used to estimate single-nucleotide polymorphism (SNP)-based heritability.
resultsFor EAA-Horvath, a genome-wide significant association was mapped to the SELP gene with the strongest SNP rs732314 (meta-GWAS: β=0.57, P=3.30×10
conclusionsWe identified novel genetic variants in the SELP gene and HLA region associated with EAA-Horvath and EAA-Hannum, respectively, among survivors of childhood cancer. The new genetic variants in combination with other replicated known variants can facilitate the identification of survivors at higher risk in developing accelerated aging and potentially inform drug targets for future intervention strategies among vulnerable survivors.
Indexed as
Identifiers
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.