Pathways of apoptosis and the modulation of cell death in cancer.
Although cell death once was viewed exclusively as the disordered, chaotic outcome of metabolic catastrophe, apoptosis now is recognized as a highly ordered, evolutionarily conserved, and genetically selected program that is essential for normal development. The death receptor pathway of apoptosis, cytotoxic T cells, prolife survival signals, Bcl-2 family of regulators, p53 and regulated cell death in cancer, and oncogenes are reviewed. Future prospects in this arena also are discussed.
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Division of Pediatric Hematology and Oncology, Children's Hospital, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
D000818:Animals; D017209:Apoptosis; D020169:Caspases / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D015854:Up-Regulation
D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D018124:Receptors, Tumor Necrosis Factor; D016159:Tumor Suppressor Protein p53; D020169:Caspases