CDK12 deficiency and the immune microenvironment in prostate cancer

Tamara L. Lotan, Emmanuel S. Antonarakis

Research output: Contribution to journalArticlepeer-review

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 languageEnglish (US)
Pages (from-to)380-382
Number of pages3
JournalClinical Cancer Research
Volume27
Issue number2
DOIs
StatePublished - Jan 15 2021
Externally publishedYes

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

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