Journal
NATURE REVIEWS CANCER
Volume 17, Issue 6, Pages 352-366Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc.2017.28
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Funding
- Cancer Research UK (CRUK) [A17341]
- Wellcome Trust [096831/Z/11/Z]
- European Research Council (ERC) [294880]
- CRUK [515818]
- CRUK Centre Network Accelerator Award on Cancer Immunotherapy (CITA) [525877]
- Manchester-UCL CRUK Lung Cancer Centre of Excellence [522434]
- National Institute for Health Research University College London Hospitals Biomedical Research Centre
- Wellcome Trust [096831/Z/11/Z] Funding Source: Wellcome Trust
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The discovery that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis of cancer cells without causing toxicity in mice has led to the in-depth study of pro-apoptotic TRAIL receptor (TRAIL-R) signalling and the development of biotherapeutic drug candidates that activate TRAIL-Rs. The outcome of clinical trials with these TRAIL-R agonists has, however, been disappointing so far. Recent evidence indicates that many cancers, in addition to being TRAIL resistant, use the endogenous TRAIL-TRAIL-R system to their own advantage. However, novel insight on two fronts - how resistance of cancer cells to TRAIL-based pro-apoptotic therapies might be overcome, and how the pro-tumorigenic effects of endogenous TRAIL might be countered - gives reasonable hope that the TRAIL system can be harnessed to treat cancer. In this Review we assess the status quo of our understanding of the biology of the TRAIL-TRAIL-R system - as well as the gaps therein - and discuss the opportunities and challenges in effectively targeting this pathway.
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