In non-hematopoietic cells such as primary fibroblasts, oncogenic RAS induces a permanent growth arrest termed senescence, which limits RAS-induced tumorigenesis in vivo [19] [23].
Most human somatic cells do not divide indefinitely but enter a terminal growth arrest termed replicative senescence.
However, vHMECs are not immortalized and eventually enter an inescapable period of growth arrest termed agonescence [ 89].
In fibroblasts and other proliferation-competent cells, a persistent DDR causes an irreversible proliferation arrest termed cellular senescence (Hayflick, 1965).
Proliferating cells can response by providing state of permanent cell cycle arrest termed cellular senescence [ 4, 5].
Most untransformed cells divide in culture for a finite number of times until they reach a state of long-term growth arrest termed senescence [ 1].
This eventually triggers cell growth arrest, termed 'replicative senescence,' via an uncapped telomere end recognized by the p53 pathway (Chin et al., 1999).
As a failsafe program in response to an oncogenic stress, cell will enter in a stable form of cell cycle arrest termed senescence.
The ensuing telomeric DDR typically leads to a permanent proliferative arrest termed cellular senescence or telomere dysfunction-induced cellular senescence (TDIS).
Normal human cells divide a limited number of times before entering an irreversible cell cycle arrest termed replicative senescence (Hayflick & Moorhead, 1961).
