Aging and Carcinogenesis

Aging and carcinogenesis are complex biological processes characterized by shared molecular and cellular mechanisms, such as the accumulation of mutations, chronic inflammation, telomere dysfunction, epigenetic alterations, and dysregulation of signaling pathways. Epidemiological data confirm a pronounced age-dependent increase in the incidence of malignant neoplasms, with solid tumors and multiple primary malignancies being more common in older patients. The article examines both agonistic (genomic instability, SASP phenotype, gut dysbiosis) and antagonistic (telomere shortening, depletion of the stem cell pool) interrelationships between aging and cancer. Particular attention is paid to promising interventional strategies, including senotherapy (senolytics and senomorphics), pharmacological approaches (metformin, rapamycin, GLP-1 receptor agonists), as well as lifestyle modulation and prehabilitation. The importance of considering biological rather than chronological age and the need for treatment personalization in elderly patients, balancing the risks of under- and overtreatment, is emphasized. In conclusion, slowing aging is considered a potentially novel avenue for the prevention of cancer.