ABSTRACT
Apoptosis is a genetically determined and normal physiologic process o f cell self-destruction that eliminates DNA-damaged or unwanted cells. Apoptosis is char acterized by condensation o f chromatin and cellular shrinkage in contrast to necrosis which is the death o f cells through injury or disease and is characterized by loss o f osmoregulation and cellular fragmentation. Regulation o f apoptosis is dependent upon the balance o f oncogene and tumor suppressor gene products. Overexpression o f tumor suppressor gene p53 arrests cell cycle progression. If D N A repair is not sufficient, the p53 gene promotes apoptosis by downregulating the bcl-2 gene. The bcl-2 gene is an oncogene that inhibits apoptosis. Members o f the bcl-2 family have been identified as both apoptotic inhibitors and promoters. Many o f the intracellular events involved in the apoptotic pathway occur in the mitochondria. Apoptosis can be triggered by withdrawal o f survival factors, by D N A damaging agents such as chemotherapy and radiation, or by activation o f natural killer cells.1
