| Literature DB >> 33199495 |
Tamara L Lotan1,2,3, Emmanuel S Antonarakis2,3.
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. ©2020 American Association for Cancer Research.Entities:
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Year: 2020 PMID: 33199495 PMCID: PMC7855343 DOI: 10.1158/1078-0432.CCR-20-3877
Source DB: PubMed Journal: Clin Cancer Res ISSN: 1078-0432 Impact factor: 13.801