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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 380-382 |
| Number of pages | 3 |
| Journal | Clinical Cancer Research |
| Volume | 27 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 15 2021 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported, in part, by the Patrick Walsh Prostate Cancer Research Fund and the NCI Cancer Center Support Grant 5P30CA006973-52 (all to E.S. Antonarakis and T.L. Lotan).
Funding Information:
T.L. Lotan reports nonfinancial support from Myriad Genetics (research sequencing) and grants from DeepBio and Roche outside the submitted work. E.S. Antonarakis reports grants and personal fees from Janssen, Sanofi, Dendreon, Merck, Bristol-Myers Squibb, AstraZeneca, and Bayer, personal
Publisher Copyright:
© 2020 American Association for Cancer Research.
Keywords
- Cyclin-Dependent Kinases
- Humans
- Male
- Prostatic Neoplasms/genetics
- T-Lymphocytes
- Tumor Microenvironment/genetics
PubMed: MeSH publication types
- Comment
- Research Support, Non-U.S. Gov't
- Journal Article
- Research Support, N.I.H., Extramural
