CDK12 Deficiency and the Immune Microenvironment in Prostate Cancer

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.

Automated summary

CDK12 inactivation in prostate cancer may generate fusion-associated neoantigens and elicit immune responses. The T-cell immune microenvironment of CDK12-deficient prostate cancers showed an increase in immunosuppressive CD4(+) FOXP3(-) T cells compared to CDK12-proficient controls.