Klin Onkol 2003; 16(6): 257-264.
Summary: Programmed cell death can be initiated upon ligand:receptor interactions at the cell surface, especially involving FasL:Fas and TRAIL:TRAIL-receptors. In various human cancers, abnormalities in the levels of these pathways have been identified in human cancer, including loss of Fas surface expression, deletion or mutation of TRAIL-Rs, and overexpression of decoy receptors or of the caspase activation inhibitor, FLIP. Apoptotic cell death triggered by ligation of Fas and TRAILRs can in some cases be connected with release of pro-apoptotic molecules from mitochondria/ER. Enhancement or reactivation of sensitivity to FasLand TRAIL-induced apoptosis in neoplastic cells contributes to chemoand radiotherapy and play a role in immunotherapeutical strategies. Furthermore, if toxicity in normal cells can be circumavented, exogenous ligands, in particular TRAIL, promise to offer a new approach in cancer therapy.
