Abstract

The accumulation of cells characteristic of neoplastic disease results from the combination of unrestrained cell growth and diminished cell death. One form of programmed cell death, apoptosis (a Greek neologism meaning “dropping off” that conjures images of leaves falling from a tree in autumn), is an important mechanism of normal cellular population control (1). Cells that are physiologically unwanted (e.g., auto-reactive lymphocytes) and cells that have suffered irreversible DNA-damaging injury (e.g., from ultraviolet light or irradiation) may be eliminated via apoptosis. Cytoreductive antineoplastic therapy operates in part by triggering apoptosis of susceptible cells (2,3).

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