Abstract
CDK12 inactivation in prostate cancer is associated with tandem genomic duplications that may generate fusion-associated neoantigens and elicit immune responses amenable to checkpoint blockade. In the first study to comprehensively characterize the T-cell immune microenvironment of CDK12-deficient prostate cancers, subsets of immunosuppressive CD4(+)FOXP3(-) T cells were increased compared with CDK12-proficient controls.See related article by Rescigno et al., p. 566.