Does senescence function as an anti-neoplastic mechanism in vivo?
Senescence has been postulated to serve as a tumor-suppressing mechanism that is responsible for limiting the replicative potential of pre-neoplastic cells. This notion, attractive in concept, remains to be proven. Senescence in one form or another certainly occurs in vitro, but the evidence that it mirrors a comparable process occurring in vivo remains elusive. Cells from older individuals do display on average shorter telomeres than do cells from younger donors (Friedrich et al., 2000; Harley et al., 1992). However, even cells obtained from centenarians contain telomeres that are sufficiently long to support further replication in vitro. (Mondello et al., 1999). Indeed, a multitude of alternative, non-telomere-based mechanisms can be invoked to explain the progressive loss of replicative potential of cells isolated from older individuals. For example, the DNA from older individuals contains more accumulated genetic damage, and some have suggested that this may be responsible for the
