Journal
CANCER RESEARCH
Volume 71, Issue 21, Pages 6567-6571Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-11-1487
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Funding
- National Health and Medical Research Council of Australia [454569]
- Peter Doherty Fellowship
- NHMRC
- Prostate Cancer Foundation of Australia, Victorian Cancer Agency
- Cancer Research Institute
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New insights into the control of T-cell activation and proliferation have led to the identification of checkpoint proteins that either up-or downmodulate T-cell reactivity. Monoclonal antibody immunotherapies that are reactive with cytotoxic T lymphocyte antigen 4 or programmed death receptor 1 have shown promising therapeutic outcomes in mice and humans with established cancer, highlighting the fact that cancer immunotherapy using T-cell checkpoint inhibitors is one of the most promising new therapeutic approaches. T-cell immunoglobulin and mucin domain 3 (TIM3) is one of many similar inhibitory molecules that are gaining attention as targets, but it remains relatively poorly studied in oncology. This review discusses our recent probing of the mechanism of action of anti-TIM3 antibody against established spontaneous and experimental tumors in mice, in the context of the exciting possibility of rationally combining agents that promote tumor-specific T-cell activation, proliferation, effector function, and survival. Cancer Res; 71(21); 6567-71. (C) 2011 AACR.
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