Apoptosis: implications of basic research for clinical oncology.
Recent studies have indicated a role for apoptosis in a variety of human diseases. Suppression of apoptosis contributes to carcinogenesis by several mechanisms, including facilitating the accumulation of gene mutations, permitting growth-factor-independent cell survival, promoting resistance to immune-based cytotoxicity, and allowing bypassing of cell-cycle checkpoints, which would normally induce apoptosis. Defects in apoptotic mechanisms also play an important part in resistance to chemotherapy and radiation. The core machinery of the cell death pathway can be reduced to a few critical types of proteins, which are well conserved across animal evolution. This review gives an update on the key players involved in apoptosis as well as an overview of the involvement of apoptosis in disease, and novel diagnostic and therapeutic options derived from the extensive basic research on this topic carried out over the last decade.
Tamm
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I
Medizinische Klinik mit Schwerpunkt Hamatologie, Onkologie, und Tumorimmunologie, Charité, Berlin, Germany. tamm@rrk-berlin.de
Schriever
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F
Dörken
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B
D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins; D000072224:Bcl-2-Like Protein 11; D002352:Carrier Proteins / Q000502:physiology; D020169:Caspases / Q000502:physiology; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D008495:Medical Oncology; D008565:Membrane Proteins; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics; D011518:Proto-Oncogene Proteins; D012106:Research
D051017:Apoptosis Regulatory Proteins; C000606775:BCL2L11 protein, human; D000072224:Bcl-2-Like Protein 11; D002352:Carrier Proteins; D006360:Heat-Shock Proteins; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D020169:Caspases