Epigenetic age acceleration contributes to long-term metabolic risk in survivors of pediatric cancer

There is an increasing need to understand the link between prior cancer treatment exposures during childhood and future health risks in long-term survivors of childhood cancer. Cardiovascular events are a leading cause of mortality in survivors; therefore, researchers are looking for modifiable pathways to target to help prevent adverse health effects. Survivors experience epigenetic age acceleration (EAA), where there is a difference between an individual’s chronological age and biological age. Survivors’ biological age acceleration is associated with a greater risk of chronological age-related health complications, such as cardiovascular disease. A study led by Zhaoming Wang, PhD, St. Jude Department of Epidemiology & Cancer Control, found EAA variably contributed to increased risk of heart attack, cardiomyopathy and abnormal glucose metabolism in the context of different cancer treatments. The study used data from the St. Jude Lifetime Cohort Study. Researchers can now investigate how anti-aging intervention strategies may slow biological age acceleration. Using these strategies, clinicians may be able to decrease the burden of cardiometabolic and cardiovascular diseases to help survivors. The study was published in the Journal of the American College of Cardiology: CardioOncology.

“This study demonstrated that accelerated aging is an underlying biological mechanism for treatment-induced cardiotoxicity. Interventions targeting accelerated aging will remediate age-related morbidity and prevent premature mortality, so ultimately healthy aging may be attainable even for survivors of childhood cancer,” said Wang.

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