Apoptosis in neuroendocrine tumours.
Acquired resistance to apoptosis in neuroendocrine tumours (NETs) may promote clonal expansion and enhance the likelihood that subsequent mutations lead to growth or persistence of the neoplastic clone. Recent studies have demonstrated that deregulation of programmed cell death may be a critical component in multistep tumourigenesis of NETs and that the frequent expression of the Bcl-2 oncoprotein in these tumours may contribute to their pathogenesis. The genetic complementation of simultaneously deregulated Bcl-2 and c-Myc may be implicated in the multistep tumourigenesis of human NETs. Furthermore, because the efficacy of cytotoxic chemotherapy relies on its ability to induce programmed cell death, resistance to apoptosis typically correlates with chemoresistance, a phenomenon that is typical in NETs. Consideration of how oncogenes affect rates of cell death, in addition to augmenting growth, has already provided valuable insights into the biology of cancer. Understanding the molecular and cellular features of this process may enable the development and application of more effective and potentially curative treatment strategies in which the induction of programmed cell death is an integral component.
Wang
D G
DG
Center for Molecular Medicine, School of Medicine, University of Connecticut Health Center, Farmington CT 06030-3101, USA. dwang@nso2.uchc.edu
D017209:Apoptosis / Q000235:genetics*; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D005786:Gene Expression Regulation; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D009154:Mutation; D018358:Neuroendocrine Tumors / Q000188:drug therapy / Q000235:genetics* / Q000503:physiopathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc