Oncogenes as regulators of apoptosis.
Although cancer is a disease that will afflict one out of three people in the Western world, when considered at a cellular level, it is a rare clonal event. Long-lived organisms, such as humans, have evolved strategies to restrict the development of potentially malignant cells, and one such mechanism is the coupling of proliferative and apoptotic pathways. Multiple oncogenes have the ability to trigger apoptosis when expressed in an inappropriate fashion, and this is thought to restrict tumour formation by eliminating potentially malignant cells that have acquired a mutation stimulating proliferation. Hence for a tumour to arise, in addition to mutations that drive proliferation, mutations that prevent apoptosis are also a prerequisite.
Medical College of Georgia, Institute of Molecular Medicine and Genetics, CB2803, 1120 15th Street, Augusta, GA 30912, U.S.A.
Mohamed
M
Labazi
Andrew C
AC
Phillips
D000818:Animals; D017209:Apoptosis; D002455:Cell Division; D004268:DNA-Binding Proteins / Q000378:metabolism; D005786:Gene Expression Regulation; D016147:Genes, Tumor Suppressor; D016259:Genes, myc / Q000502:physiology; D016158:Genes, p53 / Q000502:physiology; D006801:Humans; D051379:Mice; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation; D009687:Nuclear Proteins / Q000378:metabolism; D009857:Oncogenes / Q000502:physiology*; D015398:Signal Transduction; D015533:Transcriptional Activation; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; C000606368:Trp73 protein, mouse; D000072160:Tumor Protein p73; D025521:Tumor Suppressor Proteins