Apoptosis and Senescence

  • Martin BeckermanEmail author
Part of the Biological and Medical Physics, Biomedical Engineering book series (BIOMEDICAL)

The DNA damage checkpointing and repair responses discussed in the last chapter act as the first barrier to unrestrained cellular growth and proliferation. This barrier is raised early whenever oncogenic stimuli, that is, inappropriate cellular growth conditions, arise. Mechanistically, the unscheduled growth stimuli give rise to DNA damage and stalled replication forks. These stresses activate checkpoint pathways that halt the cell cycle to allow for time to repair the damage and restart DNA replication. If the damage is not repaired in a timely fashion, the same checkpoint-signaling elements, for example, p53 and Chk2, route the cells away from growth toward apoptosis and senescence, the later-acting barriers to cancer.

The term apoptosis was coined by Kerr, Wyllie, and Currie in 1972 to denote the process whereby cells that are damaged or no longer needed are destroyed in a systematic way through cell shrinkage, chromatin condensation, DNA fragmentation, and membrane blebbing. This...


Bcl2 Protein Replicative Senescence Heterochromatin Formation Polycomb Group Protein Senescent State 
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Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.Oak RidgeUSA

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