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Abstract

Abstract 

  1. Apoptosis is a descriptive term for the phenotype of cells undergoing programmed cell death. Apoptosis is a critical component of development and homeostasis in multicellular eukaryotic organisms. Apoptotic cell death can be distinguished from necrotic cell death by several criteria, including characteristic morphology and a minimal inflammatory reaction.

  2. The Bcl-2 family of proteins plays a central role in apoptotic control and is conserved evolutionarily. The realization that Bcl-2 functions to prevent apoptosis defined a new category of oncogene: the antiapoptotic gene. Apoptotic regulation is dependent on the relative balance of opposing Bcl-2 family members. Those family members may function by regulating homeostasis between key intracellular organelles and the cytoplasm.

  3. The caspases are evolutionarily conserved proteases that function as important mediators of apoptosis. Control of caspase activity is dependent on proteolytic processing of cytoplasmic proenzymes. Some of these proteases have autocatalytic potential. The critical downstream targets of caspase family proteolysis have not been fully defined.

  4. Many cell surface receptors, including the tumor necrosis factor receptor (TNFR) family, have been shown to modify the apoptotic sensitivity of cells. Different members of the TNFR family can promote or inhibit apoptosis. An apoptotic signaling pathway from some of these receptors has been traced by direct protein–protein interaction from receptor engagement to caspase activation.

  5. Cellular and viral oncogenes that stimulate proliferation are strong inducers of apoptosis. This induction is probably dependent on cell cycle checkpoints (tumor suppressor gene products) that detect abnormally replicating cells and trigger apoptosis. Inhibition of apoptosis therefore is frequently an essential step in the process of oncogenesis.

  6. Anticancer therapies induce apoptosis in sensitive cells. Inhibition of apoptosis is a major mechanism of chemotherapeutic resistance. Chemotherapy may accelerate the mutagenesis rate and promote aneuploidy of tumors in which apoptosis has been suppressed. New therapies directed at modifying apoptotic signaling pathways may be helpful in circumventing these problems.

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