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Discovered that blocking CTLA-4 unleashes T cells against cancer, the work behind ipilimumab and the 2018 Nobel Prize.
James Allison is Chair of the Department of Immunology and Director of the James P. Allison Institute at MD Anderson Cancer Center. An immunologist specialising in tumour immunology and T-cell biology, his 1990s work showing that CTLA-4 blockade causes tumour rejection in mice led to ipilimumab, the first checkpoint inhibitor, and he shared the 2018 Nobel Prize in Physiology or Medicine with Tasuku Honjo. His papers include the Science report on enhancement of antitumour immunity by CTLA-4 blockade and a Cell review of immune checkpoint targeting and combination strategies with curative potential. He leads the Allison Institute and the immunotherapy platform at MD Anderson, with work spanning CTLA-4, PD-1 and melanoma.
This paper launched the immunotherapy era. It was the first randomised evidence that taking a brake off the immune system could extend life in a solid cancer, and it introduced clinicians to immune-related adverse events and to responses that arrive late or after apparent progression. Ipilimumab alone has since been superseded by PD-1 antibodies and combinations, but every checkpoint programme traces back to this result.
Tumours hide from T cells by displaying PD-L1; blocking that interaction lets the immune system attack. This is the mechanism of pembrolizumab, nivolumab, atezolizumab and their relatives, which now treat more than 20 cancer types.
Every checkpoint inhibitor, from ipilimumab to pembrolizumab, rests on this idea: the immune system can already recognise cancer and just needs its brakes released. It changed the goal of immunotherapy from vaccinating against tumours to unleashing existing T cells.
Shares Leach, Krummel and Allison: releasing the CTLA-4 brake makes mice reject tumours, Hodi 2010: ipilimumab, the first checkpoint inhibitor, extends survival in metastatic melanoma, Parker Institute for Cancer Immunotherapy, CTLA-4.
Shares Hodi 2010: ipilimumab, the first checkpoint inhibitor, extends survival in metastatic melanoma, Parker Institute for Cancer Immunotherapy, CTLA-4, Ipilimumab.
Shares Hodi 2010: ipilimumab, the first checkpoint inhibitor, extends survival in metastatic melanoma, CTLA-4, Ipilimumab, PD-1.
Shares Hodi 2010: ipilimumab, the first checkpoint inhibitor, extends survival in metastatic melanoma, CTLA-4, Ipilimumab, PD-1.
Shares Hodi 2010: ipilimumab, the first checkpoint inhibitor, extends survival in metastatic melanoma, CTLA-4, Ipilimumab, PD-1.
Shares CTLA-4, Ipilimumab, PD-1, Melanoma.
Shares CTLA-4, Ipilimumab, PD-1, Melanoma.
Shares CTLA-4, Ipilimumab, PD-1, Melanoma.