What is the Origin of Therapy-Induced Senescence?

This concept emerged from cancer biology and gerontology, recognizing that cellular senescence, typically a response to oncogenic stress or telomere shortening, could also be triggered by pharmacological intervention. TIS highlights the complex, dual-edged nature of senescence, which acts as a barrier to cancer progression but also as a driver of the aging phenotype.

What is the Mechanism of Therapy-Induced Senescence?

TIS is primarily triggered by irreparable DNA damage or significant mitochondrial dysfunction caused by the therapeutic agent, which activates cell cycle inhibitory pathways like p53. The resulting senescent cells, though non-proliferative, often secrete a complex mix of pro-inflammatory molecules known as the Senescence-Associated Secretory Phenotype (SASP), which can then promote inflammation, tissue remodeling, and potentially disease recurrence in the local environment.

Therapy-Induced Senescence ∞ Area

Therapy-Induced Senescence

Meaning

Therapy-Induced Senescence (TIS) is a specific cellular response where a cell enters a state of permanent growth arrest and metabolic alteration as a direct result of exposure to a therapeutic agent, such as chemotherapy or radiation. While initially a tumor-suppressive mechanism in cancer treatment, the accumulation of these senescent cells can paradoxically contribute to local tissue toxicity and drive age-related pathologies.