The Aging-Senescence-Cancer Axis: A New Paradigm for Precision Oncology

Cellular senescence has emerged as a crucial link between aging and cancer. This phenomenon of permanent proliferation arrest occurs in response to various stresses, including DNA damage, telomere dysfunction, and oncogene activation.

While initially recognized as a tumor suppressor mechanism, senescence plays a nuanced role in cancer biology that evolves with age. The senescence-associated secretory phenotype (SASP) exemplifies this complexity. SASP factors can suppress tumor formation in young tissues but may promote cancer progression in aged environments. This duality underscores the need for age-specific strategies when targeting senescence in cancer therapy.

Senolytic drugs that selectively eliminate senescent cells have shown promise in preclinical models of aging-related conditions and cancer. In oncology, combining conventional therapies with senolysis to eliminate therapy-induced senescent cells may enhance efficacy and reduce side effects, particularly in older patients.

Alternatively, senomorphic compounds aim to suppress the detrimental effects of the SASP without killing senescent cells. Such approaches could potentially modulate the aged tumor microenvironment to impair cancer progression while preserving the beneficial aspects of senescence.

As novel therapies enter clinical testing, it is critical that oncologists familiarize themselves with the underlying biology of the aging-senescence-cancer axis.

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