ABSTRACT
Normal somatic cells invariably enter a state of permanent growth arrest and
functional decline after a finite number of divisions (1). This phenomenon,
termed cellular senescence, is believed to be a contributing factor in aging. As
we age, the organisms’ ability to withstand the erosive effects of internal and
environmental stress diminishes, rendering us vulnerable to a variety of chronic
illnesses including cancer, arthritis, diabetes, heart, and neurodegenerative
diseases (2-5). Conventional wisdom holds that the body’s decreased resistance
to stress during aging may result from the decreased efficiency of normal
maintenance and repair mechanisms. The accumulation of damage overtime may
either signal for the stimulation of antistress defense, allowing somatic cells to
survive longer but enhancing the risk of becoming cancerous, or to a cellular
surrender leading to senescence. Accordingly, senescence induction may be
considered as a barrier for cancer and thus should be exploited for the treatment
of this disease. However, the respective benefits and risks of targeting senes-
cence in cancer cells to treat tumors or in somatic cells to prevent cancer onset
must be defined. For this, it is critical to define the relationship between
senescence and cancer and characterize the molecular events eliciting these
unique cellular stress responses.
