TERT links telomere length to cancer risk by integrating genomic instability and immune modulation.
Abstract
Telomere homeostasis serves as a key regulatory mechanism linking aging and cancer. While telomere attrition imposes a proliferative barrier by inducing cellular senescence, abnormal telomere elongation circumvents this constraint, thereby granting malignant cells unlimited replicative capacity. This study systematically explores the causal relationship between telomere length and cancer risk, with the goal of elucidating the molecular pathways involved in telomere-driven tumorigenesis.
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Research summary
The paper claims that telomere length is causally linked to cancer risk through mechanisms involving genomic instability and immune modulation. This research is relevant as it addresses the underlying biological mechanisms of telomere dynamics, which are crucial for understanding aging and its relationship to cancer, potentially offering insights into longevity and age-related diseases.
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