Abstract
The concept of senescence as a barrier to tumorigenesis, either by natural replicative limits or as stress-induced senescence deserves a critical evaluation of the benefits that can be achieved for cancer diagnosis and therapy. It is accepted that neoplastic cells can be forced to undergo senescence by genetic manipulations and by epigenetic factors, including anticancer drugs, radiation and differentiating agents. Senescent features can be imposed even in the absence of the two functional effector pathways, p53 and pRb, paving the way for speculation about the possible benefits of inducing an unspecific senescence program to stop tumor growth. In the present work we will review the potential of cellular senescence to be used as target for anticancer therapy.
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