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Show abstract
After more than a century of efforts to establish cancer immunotherapy in clinical practice, the advent of checkpoint inhibition (CPI) therapy was a critical breakthrough toward this direction (Hodi et al. in Cell Rep 13(2):412–424, 2010; Wolchok et al. in N Engl J Med 369(2):122–133, 2013; Herbst et al. in Nature 515(7528):563–567, 2014; Tumeh et al. in Nature 515(7528):568–571, 2014). Further, CPIs shifted the focus from long studied shared tumor-associated antigens to mutated ones. As cancer is caused by mutations in somatic cells, the concept to utilize these correlates of ‘foreignness’ to enable recognition and lysis of the cancer cell by T cell immunity seems an obvious thing to do.