Abstract

Tumor growth is associated to chronic metabolic changes which inform the clinical phenotype and the outcome of patients with cancer. Surgery further triggers a cascade of acute neuro-immune responses leading to hypermetabolic and catabolic state. The metabolic mechanisms associated to surgical stress are well described. Preventive and therapeutic strategies have been developed, yet they appear not to benefit all surgical patients with cancer, even in the presence of a similar tumor type as well surgical procedures. Recent studies show that aging is associated with enrichment of senescent cells in different organs and tissues. Senescent cells are characterized by a specific senescence-associated secretory phenotype (SASP), which limits the potential for resilience of tissues and organs. Enhancement of the metabolic and functional recovery of patients with cancer undergoing surgery may therefore require additional therapies addressing SASP and senescent cells. Preliminary results obtained in experimental models recommend to further explore the role of senescence in mediating the metabolic changes and tissue resistance to efficient recovery.

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