An epigenome-wide association study reveals telomere length effects on lung cancer risk from smoking, suggesting important implications.
Both TL attrition and the three candidate CpGs showed significant mediation effects on lung cancer risk induced by smoking. These findings provide novel insight into the epigenetic control of telomere homeostasis mechanisms and clues for methylation alteration and TL in smoking-induced lung tumorigenesis.
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Guan et al. (2026) studied this question.
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