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Apoptosis, or programmed cell death, is the process by which a cell will actively commit suicide under tightly controlled circumstances. The apoptotic death process is associated with pronounced morphological changes in the cell as well as intranucleosomal DNA fragmentation. These criteria distinguish apoptosis from necrosis, which is cell death that occurs usually in response to physical injury. The last several years have produced an explosion of both interest in and information about apoptosis, not unlike that which occurred for the cell cycle in the 1980s. In the past, investigators did not appreciate the significance of cell death, and experiments with cell death as an outcome most often ended up in the trash. There was also a lack of molecular reagents with which to study cell death. Now, however, apoptosis is emerging as a key biological regulatory mechanism, possibly no less significant than regulation of cell growth and differentiation. Apoptosis is essential in many aspects of normal development and is required for maintaining homeostasis. Failure to regulate apoptosis negatively is associated with degenerative diseases, and failure to regulate apoptosis positively is associated with cancer and autoimmune disease. Thus, too much or to little cell death can have catastrophic consequences. Developing molecular approaches to study apoptosis in diverse systems is now the main objective of many laboratories. Some unifying themes have emerged: (1) Apoptosis may arise from incompatible or conflicting growth signals; (2) multiple pathways exist for induction of apoptosis; and (3) apoptosis can be a multistep process. This review is not meant to be comprehensive, but it is an attempt to highlight the most significant and interrelated developments presented by the participants at The Fifth Annual Pezcoller Symposium. 1
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Eileen White (1993) studied this question.
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