Cellular senescence represents a double-edged sword in cancer and its therapy. On one side, senescence-associated growth arrest and immunomodulatory properties exert potent antimalignant functions. On the other side, senescence bypass and secretory phenotype are associated with tumor progression and relapse. Recent studies have demonstrated the enormous potential to combine pro- to antisenescence interventions as a new anticancer approach. However, the heterogeneity of senescence-associated features makes definition and targeting of therapy-induced senescent cells a challenging task. Here, we describe these challenges and discuss how to exploit senescence-associated features to improve treatment efficacy and tolerability.

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