Apoptosis: A Current Molecular Analysis

Dean G TANG1, Arthur T PORTER2

1Department of Radiation Oncology, Wayne State University, Detroit, USA
2Gershenson Radiation Oncology Center, Harper Hospital, Detroit, USA


Apoptosis is a cell suicide program characterized by distinct morphological (cell shrinkage, membrane blebbing, pyknosis, chromatin margination, denser cytoplasmic images) and biochemical (e.g., DNA fragmentation into distinct ladders; degradation of apoptotic markers such as PARP and nuclear lamins) features. It is involved in multiple physiological processes examplified by involution of mammary tissues, embryonic development, homeostatic maintenance of tissues and organs, and maturation of the immune system, as well as in many pathological conditions represented by neurologic degeneration (Alzeimer's disease), autoimmune and inflammatory diseases, etiology of atherosclerosis, AIDS, and oncogenesis and tumor progression. Numerous molecular entities have been shown to regulate the apoptotic process. This review provides a concise summary of the recent data on the role of oncogenes/tumor suppressor genes, cytokines and growth factors/growth factor receptors, intracellular signal transducers, cell cycle regulators, reactive oxygen species or other free radicals, extracellular matrix regulators/cell adhesion molecules, and specific endonucleases and cytoplasmic proteases (the ICE family proteins) in regulating cell survival and apoptosis. Elucidation of the molecular mechanisms regulating apoptosis bears tremendous impact on enhancing our understanding of many diseases inflicting the human beings and undoubtedly brings us hope for the cure of these diseases. Pathology & Oncology Research, Vol 2, Nr 3, 117-131, 1996

Key words: apoptosis; genes; review

Received: Mar 5, 1996; accepted: May 12, 1996
Correspondence: Dean G TANG, Department of Radiation Oncology, Wayne State University, 407 Life Science Bldg. Detroit 48202, USA; Tel: 313-5772184, Fax: 313-5772375; E-mail:

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