Research Paper Volume 15, Issue 3 pp 617—629
Epigenetic age and lung cancer risk in the CLUE II prospective cohort study
- 1 Department of Public Health and Community Medicine, Tufts University School of Medicine, Tufts University, Boston, MA 02111, USA
- 2 Division of Nutrition Epidemiology and Data Science, Friedman School of Nutrition, Tufts University, Boston, MA 02111, USA
- 3 Department of Biostatistics and Data Science, University of Kansas Medical Center, Kansas City, KS 66160, USA
- 4 University of Kansas Cancer Center, Kansas City, KS 66160, USA
- 5 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA
- 6 The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21231, USA
- 7 Department of Epidemiology, Brown University, Providence, RI 02903, USA
- 8 Department of Pathology and Laboratory Medicine, Brown University, Providence, RI 02903, USA
Received: July 5, 2022 Accepted: January 23, 2023 Published: February 7, 2023
https://doi.org/10.18632/aging.204501How to Cite
Copyright: © 2023 Michaud et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: Epigenetic age, a robust marker of biological aging, has been associated with obesity, low-grade inflammation and metabolic diseases. However, few studies have examined associations between different epigenetic age measures and risk of lung cancer, despite great interest in finding biomarkers to assist in risk stratification for lung cancer screening.
Methods: A nested case-control study of lung cancer from the CLUE II cohort study was conducted using incidence density sampling with 1:1 matching of controls to lung cancer cases (n = 208 matched pairs). Prediagnostic blood samples were collected in 1989 (CLUE II study baseline) and stored at −70°C. DNA was extracted from buffy coat and DNA methylation levels were measured using Illumina MethylationEPIC BeadChip Arrays. Three epigenetic age acceleration (i.e., biological age is greater than chronological age) measurements (Horvath, Hannum and PhenoAge) were examined in relation to lung cancer risk using conditional logistic regression.
Results: We did not observe associations between the three epigenetic age acceleration measurements and risk of lung cancer overall; however, inverse associations for the two Hannum age acceleration measures (intrinsic and extrinsic) were observed in men and among younger participants, but not in women or older participants. We did not observe effect modification by time from blood draw to diagnosis.
Conclusion: Findings from this study do not support a positive association between three different biological age acceleration measures and risk of lung cancer. Additional studies are needed to address whether epigenetic age is associated with lung cancer in never smokers.