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CDK12 Deficiency and the Immune Microenvironment in Prostate Cancer

Tamara L Lotan1,2,3, Emmanuel S Antonarakis2,3

  • 1Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland. tlotan1@jhmi.edu.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|November 17, 2020
PubMed

Insights

CDK12 inactivation in prostate cancer drives genomic duplications, potentially creating neoantigens. This study reveals increased immunosuppressive T cells in these tumors, suggesting new avenues for immunotherapy.

Area of Science:

  • Oncology
  • Immunology
  • Genomics

Background:

  • CDK12 inactivation is observed in prostate cancer.
  • This inactivation is linked to tandem genomic duplications.
  • These duplications may lead to neoantigen generation and immune responses.

Purpose of the Study:

  • To comprehensively characterize the T-cell immune microenvironment in CDK12-deficient prostate cancers.
  • To compare the immune microenvironment of CDK12-deficient tumors with CDK12-proficient tumors.

Main Methods:

  • Analysis of the T-cell immune microenvironment.
  • Comparison of immune cell subsets between CDK12-deficient and proficient prostate cancer samples.

Main Results:

  • CDK12 inactivation is associated with tandem genomic duplications.
  • These duplications may generate fusion-associated neoantigens.
  • An increase in immunosuppressive CD4+FOXP3- T cells was observed in CDK12-deficient prostate cancers compared to controls.

Conclusions:

  • CDK12 deficiency in prostate cancer creates a unique immune microenvironment.
  • The identified immune alterations may be amenable to checkpoint blockade immunotherapy.
  • Further research into T-cell populations could inform novel therapeutic strategies.

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