Targeting cellular FLICE-like inhibitory protein as a novel approach to the treatment of Hodgkin's lymphoma.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
AbstractHodgkin's lymphoma is one of the most common lymphoid cancers, particularly among young adults. Although there have been dramatic improvements in the treatment of Hodgkin's lymphoma, leading to high cure rates in some groups, current combination chemotherapy regimes are associated with significant secondary complications in long-term survivors. Furthermore, although a proportion of patients with Hodgkin's lymphoma will be cured, there still remains a significant rate of relapse and also a smaller proportion of poor responders who will go on to die of their disease. Therefore, developments in the treatment of Hodgkin's lymphoma must be directed at improving cure rates and reducing the burden of secondary complications. In recent years, the underlying pathogenesis of Hodgkin's lymphoma has become better understood. In particular, it is emerging that a key pathogenic event in Hodgkin's lymphoma is protection from Fas-induced cell death. Recent studies by the authors' group, and others, have demonstrated that this is, in part, due to the expression by Hodgkin/Reed-Sternberg cells of the cellular Fas-associated death domain-like IL-1 converting enzyme (FLICE)-like inhibitory protein molecule, a potent inhibitor of Fas-induced death. In this review, the role of cellular FLICE-like inhibitory protein in the pathogenesis of Hodgkin's lymphoma will be explored and also the possibility of targeting this molecule in order to provide an alternative and potentially safe approach to the treatment of Hodgkin's lymphoma will be investigated.
CitationExpert Review of Anticancer Therapy, 6(6): 911-919
- Expression of the cellular FLICE-inhibitory protein (c-FLIP) protects Hodgkin's lymphoma cells from autonomous Fas-mediated death.
- Authors: Dutton A, O'Neil JD, Milner AE, Reynolds GM, Starczynski J, Crocker J, Young LS, Murray PG
- Issue date: 2004 Apr 27
- TRAF1 is involved in the classical NF-kappaB activation and CD30-induced alternative activity in Hodgkin's lymphoma cells.
- Authors: Guo F, Sun A, Wang W, He J, Hou J, Zhou P, Chen Z
- Issue date: 2009 Aug
- CCAAT/enhancer binding protein homologous protein-dependent death receptor 5 induction and ubiquitin/proteasome-mediated cellular FLICE-inhibitory protein down-regulation contribute to enhancement of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by dimethyl-celecoxib in human non small-cell lung cancer cells.
- Authors: Chen S, Liu X, Yue P, Schönthal AH, Khuri FR, Sun SY
- Issue date: 2007 Nov
- The role of cellular FLICE inhibitory protein (c-FLIP) in the pathogenesis and treatment of cancer.
- Authors: Dutton A, Young LS, Murray PG
- Issue date: 2006 Feb
- Bortezomib induces caspase-dependent apoptosis in Hodgkin lymphoma cell lines and is associated with reduced c-FLIP expression: a gene expression profiling study with implications for potential combination therapies.
- Authors: Zhao X, Qiu W, Kung J, Zhao X, Peng X, Yegappan M, Yen-Lieberman B, Hsi ED
- Issue date: 2008 Feb