Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level
TL;DR
Key aging‐related mechanisms, including genomic instability, telomere attrition, cellular senescence, chronic inflammation, chronic inflammation (inflammaging), and immune system decline, all of which create a tumor‐permissive environment are explored.
Abstract
Aging is a multifaceted biological process that profoundly influences cancer development and progression. As life expectancy increases, understanding the molecular links between aging and oncogenesis becomes crucial for developing targeted therapeutic interventions. This review explores key aging‐related mechanisms, including genomic instability, telomere attrition, cellular senescence, chronic inflammation (inflammaging), and immune system decline, all of which create a tumor‐permissive environment. The role of aging‐associated genes such as p53 , sirtuins, telomerase reverse transcriptase ( TERT ), Werner syndrome protein ( WRN ) helicase, and ataxia‐telangiectasia‐mutated (ATM) in regulating both longevity and cancer susceptibility is also discussed. Furthermore, the concept of senescence‐associated secretory phenotype (SASP) is highlighted as a double‐edged sword in cancer progression, contributing to both tumor suppression and malignancy. Additionally, biomarkers of aging relevant to cancer detection and prognosis are examined. Finally, potential therapeutic strategies, including senolytics, anti‐inflammatory treatments, and immune‐modulating approaches, are considered promising avenues to mitigate cancer risk in aging populations. A deeper understanding of aging‐related molecular pathways will aid in the development of precision oncology strategies tailored to elderly cancer patients.